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Search Results (5,946)

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Keywords = inflammation and cancer

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20 pages, 3069 KiB  
Article
Inhibitory Impact of the Amino Benzoic Derivative DAB-2-28 on the Process of Epithelial–Mesenchymal Transition in Human Breast Cancer Cells
by Laurie Fortin, Julie Girouard, Yassine Oufqir, Alexis Paquin, Francis Cloutier, Isabelle Plante, Gervais Bérubé and Carlos Reyes-Moreno
Molecules 2025, 30(15), 3284; https://doi.org/10.3390/molecules30153284 - 5 Aug 2025
Abstract
Macrophage-mediated inflammation is known to be involved in the epithelial–mesenchymal transition (EMT) of various types of cancer. This makes macrophage-derived inflammatory factors prime targets for the development of new treatments. This study uncovers the therapeutic potential and action mechanism of DAB-2-28, a small-molecule [...] Read more.
Macrophage-mediated inflammation is known to be involved in the epithelial–mesenchymal transition (EMT) of various types of cancer. This makes macrophage-derived inflammatory factors prime targets for the development of new treatments. This study uncovers the therapeutic potential and action mechanism of DAB-2-28, a small-molecule derived from para-aminobenzoic acid, in the treatment of breast cancer. The luminal MCF-7 and the triple-negative MDA-MB-231 cancer cell lines used in this study represent, respectively, breast cancers in which the differentiation states are related to the epithelial phenotype of the mammary gland and breast cancers expressing a highly aggressive mesenchymal phenotype. In MCF-7 cells, soluble factors from macrophage-conditioned media (CM-MØ) induce a characteristic morphology of mesenchymal cells with an upregulated expression of Snail1, a mesenchymal marker, as opposed to a decrease in the expression of E-cadherin, an epithelial marker. DAB-2-28 does not affect the differential expression of Snail1 and E-cadherin in response to CM-MØ, but negatively impacts other hallmarks of EMT by decreasing invasion and migration capacities, in addition to MMP9 expression and gelatinase activity, in both MCF-7 and MDA-MB-231 cells. Moreover, DAB-2-28 inhibits the phosphorylation of key pro-EMT transcriptional factors, such as NFκB, STAT3, SMAD2, CREB, and/or AKT proteins, in breast cancer cells exposed to different EMT inducers. Overall, our study provides evidence suggesting that inhibition of EMT initiation or maintenance is a key mechanism by which DAB-2-28 can exert anti-tumoral effects in breast cancer cells. Full article
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17 pages, 511 KiB  
Review
Coffee’s Impact on Health and Well-Being
by Ryan C. Emadi and Farin Kamangar
Nutrients 2025, 17(15), 2558; https://doi.org/10.3390/nu17152558 - 5 Aug 2025
Abstract
Coffee is one of the most widely consumed beverages globally, with over 60% of Americans drinking it daily. This review examines coffee’s multifaceted impact on health and well-being, drawing on decades of research. Overall, the consensus is that moderate coffee intake is more [...] Read more.
Coffee is one of the most widely consumed beverages globally, with over 60% of Americans drinking it daily. This review examines coffee’s multifaceted impact on health and well-being, drawing on decades of research. Overall, the consensus is that moderate coffee intake is more beneficial than harmful across a wide range of health outcomes. Numerous large-scale, prospective cohort studies from around the world have consistently shown that moderate coffee consumption—typically three to five cups per day—is associated with reduced overall mortality and lower risk of major diseases such as cardiovascular diseases, diabetes, stroke, respiratory conditions, cognitive decline, and potentially several types of cancer, including liver and uterine cancers. Both caffeinated and decaffeinated coffee have shown benefits. The addition of sugar and cream to coffee may attenuate coffee’s positive health effects. Despite historical concerns, coffee consumption is not linked to increased risks of cancer, hypertension, or arrhythmia. However, some concerns remain. For pregnant women, coffee consumption should be limited to lower amounts, such that the daily intake of caffeine does not exceed 200 mg/day. Also, excessive caffeinated coffee intake may cause anxiety or sleep disturbances. Coffee’s health-promoting mechanisms include improved glucose balancing, increased physical activity, increased fat oxidation, improved lung function, and reduced inflammation. Beyond mortality and chronic diseases, coffee consumption affects many aspects of well-being: it supports hydration, boosts mental acuity, enhances physical performance, and may aid bowel recovery after surgery. While the field is well-studied via long-term observational cohorts, future research should focus on randomized controlled trials, Mendelian randomization studies, and granular analyses of coffee types and additives. Full article
(This article belongs to the Section Nutritional Epidemiology)
18 pages, 1899 KiB  
Article
MALAT1 Expression Is Deregulated in miR-34a Knockout Cell Lines
by Andrea Corsi, Tonia De Simone, Angela Valentino, Elisa Orlandi, Chiara Stefani, Cristina Patuzzo, Stefania Fochi, Maria Giusy Bruno, Elisabetta Trabetti, John Charles Rotondo, Chiara Mazziotta, Maria Teresa Valenti, Alessandra Ruggiero, Donato Zipeto, Cristina Bombieri and Maria Grazia Romanelli
Non-Coding RNA 2025, 11(4), 60; https://doi.org/10.3390/ncrna11040060 - 5 Aug 2025
Abstract
Background/Objectives: Non-coding microRNA-34a (miR-34a) regulates the expression of key factors involved in several cellular processes, such as differentiation, apoptosis, proliferation, cell cycle, and senescence. Deregulation of the expression of these factors is implicated in the onset and progression of several human diseases, including [...] Read more.
Background/Objectives: Non-coding microRNA-34a (miR-34a) regulates the expression of key factors involved in several cellular processes, such as differentiation, apoptosis, proliferation, cell cycle, and senescence. Deregulation of the expression of these factors is implicated in the onset and progression of several human diseases, including cancer, neurodegenerative disorders, and pathologies associated with viral infections and inflammation. Despite numerous studies, the molecular mechanisms regulated by miR-34a remain to be fully understood. The present study aimed to generate miR-34a knockout cell lines to identify novel genes potentially regulated by its expression. Methods: We employed the CRISPR-Cas9 gene editing system to knock out the hsa-miR-34a gene in HeLa and 293T cell lines, two widely used models for studying molecular and cellular mechanisms. We compared proliferation rates and gene expression profiles via RNA-seq and qPCR analyses between the wild-type and miR-34a KO cell lines. Results: Knockout of miR-34a resulted in a decreased proliferation rate in both cell lines. Noteworthy, the ablation of miR-34a resulted in increased expression of the long non-coding RNA MALAT1. Additionally, miR-34a-5p silencing in the A375 melanoma cell line led to MALAT1 overexpression. Conclusions: Our findings support the role of the miR-34a/MALAT1 axis in regulating proliferation processes. Full article
(This article belongs to the Section Long Non-Coding RNA)
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27 pages, 2559 KiB  
Review
Virgin Coconut Oil and Its Lauric Acid, Between Anticancer Activity and Modulation of Chemotherapy Toxicity: A Review
by Debalina Bose, Adetayo Olorunlana, Rania Abdel-Latif, Ademola C. Famurewa and Eman M. Othman
J. Xenobiot. 2025, 15(4), 126; https://doi.org/10.3390/jox15040126 - 5 Aug 2025
Abstract
Virgin coconut oil (VCO) has emerged as a functional food oil with considerable health benefits and wide applications in the food, pharmaceutical, and cosmetic industries due to its resident bioactive compounds, including lauric acid (LA). LA is the most abundant saturated medium-chain fatty [...] Read more.
Virgin coconut oil (VCO) has emerged as a functional food oil with considerable health benefits and wide applications in the food, pharmaceutical, and cosmetic industries due to its resident bioactive compounds, including lauric acid (LA). LA is the most abundant saturated medium-chain fatty acid in VCO and has been associated with several pharmacological activities. The literatures show the pharmacological effects of VCO and LA on chronic pathologies, infectious diseases, and metabolic disorders. A robust body of evidence shows that LA and other phenolic compounds are responsible for the VCO protection against toxicities and pharmacological efficacies. This review elucidates the anticancer mechanisms of VCO/LA and their modulation of the chemotherapy-induced side effect toxicity. VCO, LA, and their nanomaterial/encapsulated derivatives promote ROS generation, antiproliferation, apoptosis, cell cycle arrest, the inhibition of metastasis, and the modulation of cancer-related signaling pathways for cancer cell death in vivo and in vitro. VCO mitigates oxidative inflammation and apoptosis to block the underlying mechanisms of the side effect toxicity of chemotherapy. However, the possible beneficial effect of LA on the toxicity of chemotherapy is currently unknown. The available evidence emphasizes the anticancer effect and mechanism of VCO and LA, and the VCO potential to combat adverse side effects of chemotherapy. Thus, VCO and LA are potential adjuvant therapeutic agents in the management of various cancers. Nevertheless, future studies should be targeted at elucidating cancer-related molecular mechanisms to bridge the gap in knowledge. Full article
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16 pages, 2235 KiB  
Article
Plasma Lysophosphatidylcholine Levels Correlate with Prognosis and Immunotherapy Response in Squamous Cell Carcinoma
by Tomoyuki Iwasaki, Hidekazu Shirota, Eiji Hishinuma, Shinpei Kawaoka, Naomi Matsukawa, Yuki Kasahara, Kota Ouchi, Hiroo Imai, Ken Saijo, Keigo Komine, Masanobu Takahashi, Chikashi Ishioka, Seizo Koshiba and Hisato Kawakami
Int. J. Mol. Sci. 2025, 26(15), 7528; https://doi.org/10.3390/ijms26157528 (registering DOI) - 4 Aug 2025
Abstract
Cancer is a systemic disease rather than a localized pathology and is characterized by widespread effects, including whole-body exhaustion and chronic inflammation. A thorough understanding of cancer pathophysiology requires a systemic approach that accounts for the complex interactions between cancer cells and host [...] Read more.
Cancer is a systemic disease rather than a localized pathology and is characterized by widespread effects, including whole-body exhaustion and chronic inflammation. A thorough understanding of cancer pathophysiology requires a systemic approach that accounts for the complex interactions between cancer cells and host tissues. To explore these dynamics, we employed a comprehensive metabolomic analysis of plasma samples from patients with either esophageal or head and neck squamous cell carcinoma (SCC). Plasma samples from 149 patients were metabolically profiled and correlated with clinical data. Among the metabolites identified, lysophosphatidylcholine (LPC) emerged as the sole biomarker strongly correlated with prognosis. A significant reduction in plasma LPC levels was linked to poorer overall survival. Plasma LPC levels demonstrated minimal correlation with patient-specific factors, such as tumor size and general condition, but showed significant association with the response to immune checkpoint inhibitor therapy. Proteomic and cytokine analyses revealed that low plasma LPC levels reflected systemic chronic inflammation, characterized by high levels of inflammatory proteins, the cytokines interleukin-6 and tumor necrosis factor-α, and coagulation-related proteins. These findings indicate that plasma LPC levels may be used as reliable biomarkers for predicting prognosis and evaluating the efficacy of immunotherapy in patients with SCC. Full article
(This article belongs to the Special Issue Molecular Diagnostics and Genomics of Tumors)
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15 pages, 8600 KiB  
Article
A Small-Molecule Compound Targeting Canine Mammary Cancer Regulates CXCL10 and MECOM Transcripts via Histone Modifications in CMT-N7
by Rongrong Wang, Chuyang Zhu, Xiaoyue Yuan, Cuipeng Zhu, Saber Y. Adam, Haoyu Liu, Demin Cai and Jiaguo Liu
Animals 2025, 15(15), 2274; https://doi.org/10.3390/ani15152274 - 4 Aug 2025
Abstract
Nuclear receptors are involved in multiple biological processes, among which RORγ can regulate the expression of inflammation-related genes and is thus frequently used as a therapeutic target for cancer. Canine mammary cancer is one of the most common tumor diseases in dogs, with [...] Read more.
Nuclear receptors are involved in multiple biological processes, among which RORγ can regulate the expression of inflammation-related genes and is thus frequently used as a therapeutic target for cancer. Canine mammary cancer is one of the most common tumor diseases in dogs, with a relative incidence rate of 46.71% for CMT in China over the past five years, severely threatening the life and health of dogs. Therefore, the search for novel drugs targeting canine mammary cancer is of great significance. This study aims to investigate how the RORγ inhibitors W6134 and XY018 affect the expression of inflammatory genes through histone modifications in CMT-N7 cells. These results show that W6134 and XY018 can upregulate signaling pathways related to inflammation and apoptosis and influence the expression of associated genes. The close link between RORγ and inflammation-related genes further confirms that RORγ may serve as a therapeutic target for canine cancer. Additionally, ChIP-qPCR was used to detect the enrichment of histone markers such as P300, H3K27ac, H3K4me1, H3K9la, and H3K9bhb at the target loci of CXCL10 and MECOM genes. Collectively, our findings provide molecular evidence for the protective role of RORγ in canine mammary cancer, potentially by regulating inflammatory pathways via histone modifications, offering new insights for improving the cure rate and survival of affected dogs. Full article
(This article belongs to the Special Issue Nutrition, Physiology and Metabolism of Companion Animals)
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14 pages, 1732 KiB  
Article
A Promising Prognostic Indicator for Pleural Mesothelioma: Pan-Immuno-Inflammation Value
by Serkan Yaşar, Feride Yılmaz, Ömer Denizhan Tatar, Hasan Çağrı Yıldırım, Zafer Arık, Şuayib Yalçın and Mustafa Erman
J. Clin. Med. 2025, 14(15), 5467; https://doi.org/10.3390/jcm14155467 - 4 Aug 2025
Abstract
Background: Pleural mesothelioma (PM) is a type of cancer that is difficult to diagnose and treat. Patients may have vastly varying prognoses, and prognostic factors may help guide the clinical approach. As a recently identified biomarker, the pan-Immune-Inflammation-Value (PIV) is a simple, comprehensive, [...] Read more.
Background: Pleural mesothelioma (PM) is a type of cancer that is difficult to diagnose and treat. Patients may have vastly varying prognoses, and prognostic factors may help guide the clinical approach. As a recently identified biomarker, the pan-Immune-Inflammation-Value (PIV) is a simple, comprehensive, and peripheral blood cell-based biomarker. Methods: The present study represents a retrospective observational analysis carried out within a single-center setting. Ninety-five patients with PM stages I–IV were enrolled in the study. We analyzed the correlation between patients’ demographic characteristics, clinicopathological factors such as histological subtypes, surgery status, tumor thickness, blood-based parameters, and treatment options with their prognoses. PIV was calculated by the following formula: (neutrophil count × monocyte count × platelet count)/lymphocyte count. Additionally, blood-based parameters were used to calculate the platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and systemic immune inflammation index (SII). Results: We categorized the patients into two groups, low PIV group (PIV ≤ 732.3) and high PIV group (PIV > 732.3) according to the determined cut-off value, which was defined as the median. It was revealed that high PIV was associated with poor survival outcomes. The median follow-up period was 15.8 months (interquartile range, IQR, 7.1 to 29.8 months). The median overall survival (OS) was significantly longer in patients in the low PIV group (median 29.8 months, 95% confidence interval (CI), 15.6 to 44) than the high PIV group (median 14.7 months, 95% CI, 10.8 to 18.6 p < 0.001). Furthermore, the study revealed that patients with low PIV, NLR, and SII values were more likely to be eligible for surgery and were diagnosed at earlier stages. Additionally, these markers were identified as potential predictors of disease-free survival (DFS) in the surgical cohort and of treatment response across the entire patient population. Conclusions: In addition to well-established clinical factors such as stage, histologic subtype, resectability, and Eastern Cooperative Oncology Group (ECOG) performance status (PS), PIV emerged as an independent and significant prognostic factor of overall survival (OS) in patients with PM. Moreover, PIV also demonstrated a remarkable independent prognostic value for disease-free survival (DFS) in this patient population. Additionally, some clues are provided for conditions such as treatment responses, staging, and suitability for surgery. As such, in this cohort, it has outperformed the other blood-based markers based on our findings. Given its ease of calculation and cost-effectiveness, PIV represents a promising and practical prognostic tool in the clinical management of pleural mesothelioma. It can be easily calculated using routinely available laboratory parameters for every cancer patient, requiring no additional cost or complex procedures, thus facilitating its integration into everyday clinical practice. Full article
(This article belongs to the Section Oncology)
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33 pages, 1872 KiB  
Review
Exploring the Epidemiologic Burden, Pathogenetic Features, and Clinical Outcomes of Primary Liver Cancer in Patients with Type 2 Diabetes Mellitus (T2DM) and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Scoping Review
by Mario Romeo, Fiammetta Di Nardo, Carmine Napolitano, Claudio Basile, Carlo Palma, Paolo Vaia, Marcello Dallio and Alessandro Federico
Diabetology 2025, 6(8), 79; https://doi.org/10.3390/diabetology6080079 (registering DOI) - 4 Aug 2025
Abstract
Background/Objectives: Primary liver cancer (PLC), encompassing hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), constitutes a growing global health concern. Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) and Type 2 diabetes mellitus (T2DM) represent a recurrent epidemiological overlap. Individuals with MASLD and T2DM (MASLD-T2DM) are [...] Read more.
Background/Objectives: Primary liver cancer (PLC), encompassing hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), constitutes a growing global health concern. Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) and Type 2 diabetes mellitus (T2DM) represent a recurrent epidemiological overlap. Individuals with MASLD and T2DM (MASLD-T2DM) are at a higher risk of PLC. This scoping review highlights the epidemiological burden, the classic and novel pathogenetic frontiers, and the potential strategies optimizing the management of PLC in MASLD-T2DM. Methods: A systematic search of the PubMed, Medline, and SCOPUS electronic databases was conducted to identify evidence investigating the pathogenetic mechanisms linking MASLD and T2DM to hepatic carcinogenesis, highlighting the most relevant targets and the relatively emerging therapeutic strategies. The search algorithm included in sequence the filter words: “MASLD”, “liver steatosis”, “obesity”, “metabolic syndrome”, “body composition”, “insulin resistance”, “inflammation”, “oxidative stress”, “metabolic dysfunction”, “microbiota”, “glucose”, “immunometabolism”, “trained immunity”. Results: In the MASD-T2DM setting, insulin resistance (IR) and IR-induced mechanisms (including chronic inflammation, insulin/IGF-1 axis dysregulation, and autophagy), simultaneously with the alterations of gut microbiota composition and functioning, represent crucial pathogenetic factors in hepatocarcinogenesis. Besides, the glucose-related metabolic reprogramming emerged as a crucial pathogenetic moment contributing to cancer progression and immune evasion. In this scenario, lifestyle changes, simultaneously with antidiabetic drugs targeting IR-related effects and gut-liver axis, in parallel with novel approaches modulating immunometabolic pathways, represent promising strategies. Conclusions: Metabolic dysfunction, classically featuring MASLD-T2DM, constitutes a continuously expanding global issue, as well as a critical driver in PLC progression, demanding integrated and personalized interventions to reduce the future burden of disease. Full article
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21 pages, 632 KiB  
Review
DNA Methylation in Bladder Cancer: Diagnostic and Therapeutic Perspectives—A Narrative Review
by Dragoş Puia, Marius Ivănuță and Cătălin Pricop
Int. J. Mol. Sci. 2025, 26(15), 7507; https://doi.org/10.3390/ijms26157507 (registering DOI) - 3 Aug 2025
Viewed by 60
Abstract
Bladder cancer pathogenesis is closely linked to epigenetic alterations, particularly DNA methylation and demethylation processes. Environmental carcinogens and persistent inflammatory stimuli—such as recurrent urinary tract infections—can induce aberrant DNA methylation, altering gene expression profiles and contributing to malignant transformation. This review synthesizes current [...] Read more.
Bladder cancer pathogenesis is closely linked to epigenetic alterations, particularly DNA methylation and demethylation processes. Environmental carcinogens and persistent inflammatory stimuli—such as recurrent urinary tract infections—can induce aberrant DNA methylation, altering gene expression profiles and contributing to malignant transformation. This review synthesizes current evidence on the role of DNA methyltransferases (DNMT1, DNMT3a, DNMT3b) and the hypermethylation of key tumour suppressor genes, including A2BP1, NPTX2, SOX11, PENK, NKX6-2, DBC1, MYO3A, and CA10, in bladder cancer. It also evaluates the therapeutic application of DNA-demethylating agents such as 5-azacytidine and highlights the impact of chronic inflammation on epigenetic regulation. Promoter hypermethylation of tumour suppressor genes leads to transcriptional silencing and unchecked cell proliferation. Urine-based DNA methylation assays provide a sensitive and specific method for non-invasive early detection, with single-target approaches offering high diagnostic precision. Animal models are increasingly employed to validate these findings, allowing the study of methylation dynamics and gene–environment interactions in vivo. DNA methylation represents a key epigenetic mechanism in bladder cancer, with significant diagnostic, prognostic, and therapeutic implications. Integration of human and experimental data supports the use of methylation-based biomarkers for early detection and targeted treatment, paving the way for personalized approaches in bladder cancer management. Full article
(This article belongs to the Section Molecular Oncology)
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28 pages, 1674 KiB  
Review
Mechanism of RCD and the Role of Different Death Signaling Pathways in Cancer
by Jianming Zhou, Ruotong Huang, Maidinai Aimaiti, Qingyu Zhou, Xiang Wu, Jiajun Zhu, Xiangyi Ma, Ke Qian, Qi Zhou, Lianlong Hu, Xiaoyi Yang, Yiting Tang, Yong Lin and Shuying Chen
Biomedicines 2025, 13(8), 1880; https://doi.org/10.3390/biomedicines13081880 - 2 Aug 2025
Viewed by 258
Abstract
Cancer remains a significant global health challenge, with China being particularly affected because of its large population. Regulated cell death (RCD) mechanisms, including autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis, play complex roles in cancer development and progression. This review explores the dual roles [...] Read more.
Cancer remains a significant global health challenge, with China being particularly affected because of its large population. Regulated cell death (RCD) mechanisms, including autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis, play complex roles in cancer development and progression. This review explores the dual roles of autophagy and apoptosis in cancer, highlighting their tumor-suppressive and tumor-promoting functions. Autophagy can maintain genomic stability, induce apoptosis, and suppress protumor inflammation, but it may also support tumor cell survival and drug resistance. Apoptosis, while primarily tumor-suppressive, can paradoxically promote cancer progression in certain contexts. Other RCD mechanisms, such as necroptosis, pyroptosis, and ferroptosis, also exhibit dual roles in cancer, influencing tumor growth, metastasis, and immune responses. Understanding these mechanisms is crucial for developing targeted cancer therapies. This review provides insights into the intricate interplay between RCD mechanisms and cancer, emphasizing the need for context-dependent therapeutic strategies. Full article
(This article belongs to the Special Issue Autophagy, Apoptosis and Cancer: 2025 Update)
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30 pages, 1428 KiB  
Review
The Oral–Gut Microbiota Axis Across the Lifespan: New Insights on a Forgotten Interaction
by Domenico Azzolino, Margherita Carnevale-Schianca, Luigi Santacroce, Marica Colella, Alessia Felicetti, Leonardo Terranova, Roberto Carlos Castrejón-Pérez, Franklin Garcia-Godoy, Tiziano Lucchi and Pier Carmine Passarelli
Nutrients 2025, 17(15), 2538; https://doi.org/10.3390/nu17152538 - 1 Aug 2025
Viewed by 147
Abstract
The oral–gut microbiota axis is a relatively new field of research. Although most studies have focused separately on the oral and gut microbiota, emerging evidence has highlighted that the two microbiota are interconnected and may influence each other through various mechanisms shaping systemic [...] Read more.
The oral–gut microbiota axis is a relatively new field of research. Although most studies have focused separately on the oral and gut microbiota, emerging evidence has highlighted that the two microbiota are interconnected and may influence each other through various mechanisms shaping systemic health. The aim of this review is therefore to provide an overview of the interactions between oral and gut microbiota, and the influence of diet and related metabolites on this axis. Pathogenic oral bacteria, such as Porphyromonas gingivalis and Fusobacterium nucleatum, can migrate to the gut through the enteral route, particularly in individuals with weakened gastrointestinal defenses or conditions like gastroesophageal reflux disease, contributing to disorders like inflammatory bowel disease and colorectal cancer. Bile acids, altered by gut microbes, also play a significant role in modulating these microbiota interactions and inflammatory responses. Oral bacteria can also spread via the bloodstream, promoting systemic inflammation and worsening some conditions like cardiovascular disease. Translocation of microorganisms can also take place from the gut to the oral cavity through fecal–oral transmission, especially within poor sanitary conditions. Some metabolites including short-chain fatty acids, trimethylamine N-oxide, indole and its derivatives, bile acids, and lipopolysaccharides produced by both oral and gut microbes seem to play central roles in mediating oral–gut interactions. The complex interplay between oral and gut microbiota underscores their crucial role in maintaining systemic health and highlights the potential consequences of dysbiosis at both the oral and gastrointestinal level. Some dietary patterns and nutritional compounds including probiotics and prebiotics seem to exert beneficial effects both on oral and gut microbiota eubiosis. A better understanding of these microbial interactions could therefore pave the way for the prevention and management of systemic conditions, improving overall health outcomes. Full article
(This article belongs to the Special Issue Exploring the Lifespan Dynamics of Oral–Gut Microbiota Interactions)
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13 pages, 1770 KiB  
Article
Inhibitory Effects of 3-Deoxysappanchalcone on Particulate-Matter-Induced Pulmonary Injury
by Chang-Woo Ryu, Jinhee Lee, Gyuri Han, Jin-Young Lee and Jong-Sup Bae
Curr. Issues Mol. Biol. 2025, 47(8), 608; https://doi.org/10.3390/cimb47080608 - 1 Aug 2025
Viewed by 92
Abstract
Fine particulate matter (PM2.5) exposure has been linked to increased lung damage due to compromised vascular barrier function, while 3-deoxysappanchalcone (3-DSC), a chalcone derived from Caesalpinia sappan, is known for its pharmacological benefits such as anti-cancer, anti-inflammatory, and antioxidant effects; [...] Read more.
Fine particulate matter (PM2.5) exposure has been linked to increased lung damage due to compromised vascular barrier function, while 3-deoxysappanchalcone (3-DSC), a chalcone derived from Caesalpinia sappan, is known for its pharmacological benefits such as anti-cancer, anti-inflammatory, and antioxidant effects; however, its potential role in mitigating PM2.5-induced pulmonary damage remains unexplored. To confirm the inhibitory effects of 3-DSC on PM2.5-induced pulmonary injury, this research focused on evaluating how 3-DSC influences PM2.5-induced disruption of the barrier of the endothelial cells (ECs) in the lungs and the resulting pulmonary inflammation. Permeability, leukocyte migration, proinflammatory protein activation, reactive oxygen species (ROS) generation, and histology were assessed in PM2.5-treated ECs and mice. This study demonstrated that 3-DSC effectively neutralized the reactive oxygen species (ROS) generated by PM2.5 exposure in the lung endothelial cells, suppressing ROS-triggered p38 MAPK activation while enhancing Akt signaling pathways critical to preserving vascular barrier function. In animal models, 3-DSC administration markedly decreased vascular permeability, attenuated the influx of immune cells into the lung tissue, and lowered inflammatory mediators like cytokines in the airways of PM2.5-exposed mice. These data suggest that 3-DSC might exert protective effects on PM2.5-induced inflammatory lung injury and vascular hyperpermeability. Full article
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18 pages, 1894 KiB  
Article
Are Calculated Immune Markers with or Without Comorbidities Good Predictors of Colorectal Cancer Survival? The Results of a Longitudinal Study
by Zoltan Herold, Magdolna Herold, Gyongyver Szentmartoni, Reka Szalasy, Julia Lohinszky, Aniko Somogyi, Attila Marcell Szasz and Magdolna Dank
Med. Sci. 2025, 13(3), 108; https://doi.org/10.3390/medsci13030108 - 1 Aug 2025
Viewed by 76
Abstract
Background/Objectives: Although numerous prognostic biomarkers have been proposed for colorectal cancer (CRC), their longitudinal evaluation remains limited. The aim of this study was to investigate longitudinal changes in biomarkers calculated from routinely used laboratory markers and their relationships to common chronic diseases (comorbidities). [...] Read more.
Background/Objectives: Although numerous prognostic biomarkers have been proposed for colorectal cancer (CRC), their longitudinal evaluation remains limited. The aim of this study was to investigate longitudinal changes in biomarkers calculated from routinely used laboratory markers and their relationships to common chronic diseases (comorbidities). Methods: A retrospective longitudinal observational study was completed with the inclusion of 817 CRC patients and a total of 4542 measurement points. Pan-immune inflammation value (PIV), prognostic nutritional index (PNI), and systemic immune-inflammation index (SII) were calculated based on complete blood count and albumin measurement data. Results: Longitudinal data analyses confirmed the different values and slopes of the parameters tested at the different endpoints. Survivors had the lowest and most constant PIVs and SII values, and the highest and most slowly decreasing PNI values. Those patients with non-cancerous death had similar values to the previous cohort, but an increase/decrease occurred towards the death event. Patients with CRC-related death had significantly higher PIVs and SII values and significantly lower PNI values (p < 0.0001), and a significant increase/decrease was observed at the early observational periods. The presence of lymph node and/or distant metastases, adjuvant chemotherapy, and hypertension significantly affected PIVs and SII and/or PNI values. The changes in PIVs and SII and PNI values toward pathological values are poor prognostic signs (p < 0.0001). Conclusions: Each of the three calculated markers demonstrates suitability for longitudinal patient follow-up, and their pathological alterations over time serve as valuable prognostic indicators. They may also be useful to detect certain clinicopathological parameters early. Full article
(This article belongs to the Section Cancer and Cancer-Related Research)
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16 pages, 19172 KiB  
Communication
DEAD-Box Helicase 3 Modulates the Non-Coding RNA Pool in Ribonucleoprotein Condensates During Stress Granule Formation
by Elizaveta Korunova, B. Celia Cui, Hao Ji, Aliaksandra Sikirzhytskaya, Srestha Samaddar, Mengqian Chen, Vitali Sikirzhytski and Michael Shtutman
Non-Coding RNA 2025, 11(4), 59; https://doi.org/10.3390/ncrna11040059 - 1 Aug 2025
Viewed by 156
Abstract
Stress granule formation is a type of liquid–liquid phase separation in the cytoplasm, leading to RNA–protein condensates that are associated with various cellular stress responses and implicated in numerous pathologies, including cancer, neurodegeneration, inflammation, and cellular senescence. One of the key components of [...] Read more.
Stress granule formation is a type of liquid–liquid phase separation in the cytoplasm, leading to RNA–protein condensates that are associated with various cellular stress responses and implicated in numerous pathologies, including cancer, neurodegeneration, inflammation, and cellular senescence. One of the key components of mammalian stress granules is the DEAD-box RNA helicase DDX3, which unwinds RNA in an ATP-dependent manner. DDX3 is involved in multiple steps of RNA metabolism, facilitating gene transcription, splicing, and nuclear export and regulating cytoplasmic translation. In this study, we investigate the role of the RNA helicase DDX3’s enzymatic activity in shaping the RNA content of ribonucleoprotein (RNP) condensates formed during arsenite-induced stress by inhibiting DDX3 activity with RK-33, a small molecule previously shown to be effective in cancer clinical studies. Using the human osteosarcoma U2OS cell line, we purified the RNP granule fraction and performed RNA sequencing to assess changes in the RNA pool. Our results reveal that RK-33 treatment alters the composition of non-coding RNAs within the RNP granule fraction. We observed a DDX3-dependent increase in circular RNA (circRNA) content and alterations in the granule-associated intronic RNAs, suggesting a novel role for DDX3 in regulating the cytoplasmic redistribution of non-coding RNAs. Full article
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14 pages, 1813 KiB  
Article
Elevated Antigen-Presenting-Cell Signature Genes Predict Stemness and Metabolic Reprogramming States in Glioblastoma
by Ji-Yong Sung and Kihwan Hwang
Int. J. Mol. Sci. 2025, 26(15), 7411; https://doi.org/10.3390/ijms26157411 - 1 Aug 2025
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Abstract
Glioblastoma (GBM) is a highly aggressive and heterogeneous brain tumor. Glioma stem-like cells (GSCs) play a central role in tumor progression, therapeutic resistance, and recurrence. Although immune cells are known to shape the GBM microenvironment, the impact of antigen-presenting-cell (APC) signature genes on [...] Read more.
Glioblastoma (GBM) is a highly aggressive and heterogeneous brain tumor. Glioma stem-like cells (GSCs) play a central role in tumor progression, therapeutic resistance, and recurrence. Although immune cells are known to shape the GBM microenvironment, the impact of antigen-presenting-cell (APC) signature genes on tumor-intrinsic phenotypes remains underexplored. We analyzed both bulk- and single-cell RNA sequencing datasets of GBM to investigate the association between APC gene expression and tumor-cell states, including stemness and metabolic reprogramming. Signature scores were computed using curated gene sets related to APC activity, KEGG metabolic pathways, and cancer hallmark pathways. Protein–protein interaction (PPI) networks were constructed to examine the links between immune regulators and metabolic programs. The high expression of APC-related genes, such as HLA-DRA, CD74, CD80, CD86, and CIITA, was associated with lower stemness signatures and enhanced inflammatory signaling. These APC-high states (mean difference = –0.43, adjusted p < 0.001) also showed a shift in metabolic activity, with decreased oxidative phosphorylation and increased lipid and steroid metabolism. This pattern suggests coordinated changes in immune activity and metabolic status. Furthermore, TNF-α and other inflammatory markers were more highly expressed in the less stem-like tumor cells, indicating a possible role of inflammation in promoting differentiation. Our findings revealed that elevated APC gene signatures are associated with more differentiated and metabolically specialized GBM cell states. These transcriptional features may also reflect greater immunogenicity and inflammation sensitivity. The APC metabolic signature may serve as a useful biomarker to identify GBM subpopulations with reduced stemness and increased immune engagement, offering potential therapeutic implications. Full article
(This article belongs to the Special Issue Advanced Research on Cancer Stem Cells)
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