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Search Results (2,706)

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Keywords = post-transcriptional regulations

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24 pages, 6891 KiB  
Article
Gestational and Lactation Exposure to Perfluorohexanoic Acid Results in Sex-Specific Changes in the Cerebellum in Mice
by Elizabeth C. Plunk, Navya Navnith, Hannah Swan, Linh Le, Matthew McCall, Marissa E. Sobolewski and Ania K. Majewska
Int. J. Mol. Sci. 2025, 26(16), 8008; https://doi.org/10.3390/ijms26168008 - 19 Aug 2025
Abstract
Currently regulated per- and polyfluoroalkyl substances (PFAS) have been associated with immune, endocrine, and neurotoxicity following gestational exposures. As a result, industries have effectively replaced them with next-generation PFAS, including perfluorohexanoic acid (PFHxA). PFHxA is increasingly found in the serum of pregnant women [...] Read more.
Currently regulated per- and polyfluoroalkyl substances (PFAS) have been associated with immune, endocrine, and neurotoxicity following gestational exposures. As a result, industries have effectively replaced them with next-generation PFAS, including perfluorohexanoic acid (PFHxA). PFHxA is increasingly found in the serum of pregnant women and in breast milk, and adult human post-mortem studies indicate that PFHxA is found in the brain, with the highest concentrations in the cerebellum and hypothalamus. Despite evidence of gestational, lactational, and nervous system exposure to PFHxA, developmental neurotoxicity (DNT) testing in mammals has not been conducted. For DNT evaluation, we exposed pregnant C57Bl/6J mice daily from gestational day 0 through postnatal day (P) 21 to two PFHxA exposure levels (a lower (0.32 mg/kg of body weight (bw), or higher (50 mg/kg of bw) dose of PFHxA)) or ddH2O using treat-based administration. Given the high PFHxA levels in the cerebellum in post-mortem studies and the cerebellum’s protracted developmental window, we assessed acute transcriptional dysregulation and cellular morphology in this brain region on the last day of exposure at P21. Using bulk-RNA sequencing, we found that PFHxA exposure had subtle effects on transcripts related to neurons and glia, with females having a greater number of dysregulated transcripts than males. Using immunohistochemistry, we found that Purkinje cell linear frequency was increased in specific lobules in the higher-exposure group and that microglial morphology underwent subtle changes in specific cerebellar layers in the lower-exposure group in both sexes. Together these data suggest that PFHxA exposure may have lobule-specific impacts on the development of both neurons and glia in the cerebellum, highlighting the importance of studying the neurotoxicity of PFHxA in both sexes. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants: 2nd Edition)
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20 pages, 1024 KiB  
Review
Partners in Silencing: Decoding the Mammalian Argonaute Interactome
by Srinaath Narasimhan and Stefan J. Erkeland
Non-Coding RNA 2025, 11(4), 62; https://doi.org/10.3390/ncrna11040062 - 19 Aug 2025
Abstract
MicroRNAs (miRNAs) are key post-transcriptional regulators controlling gene expression across several cellular processes, including development, proliferation, and apoptosis. Their biogenesis involves a multi-step pathway, including the processing of primary transcripts and the assembly of the RNA-Induced Silencing Complex (RISC) with Argonaute (AGO) proteins [...] Read more.
MicroRNAs (miRNAs) are key post-transcriptional regulators controlling gene expression across several cellular processes, including development, proliferation, and apoptosis. Their biogenesis involves a multi-step pathway, including the processing of primary transcripts and the assembly of the RNA-Induced Silencing Complex (RISC) with Argonaute (AGO) proteins at its core. This review provides a comprehensive overview of the molecular dynamics of miRNA-loaded RISC (miRISC), focusing on the post-translational modifications, the interactors of AGOs and the mechanisms that fine-tune and coordinate miRISC activity. The composition of miRISC influences AGO stability, localization, and silencing efficiency, thereby maintaining cellular homeostasis and development and mediating the response to various types of cellular stress. Uncommon regulatory mechanisms, including AGO modifications during, e.g., hypoxia or Type 2 T cell responses and miRISC functionality, with myriad RNA-binding proteins (RBPs), will be discussed. This review aims at highlighting the recent advances in the understanding of the intricate regulation of miRISC-driven gene silencing. Full article
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24 pages, 3157 KiB  
Review
The Roles of RNA-Binding Proteins in Vasculogenic Mimicry Regulation in Glioblastoma
by Pok Kong Tsoi, Xian Liu, Man Ding Wong and Liang-Ting Lin
Int. J. Mol. Sci. 2025, 26(16), 7976; https://doi.org/10.3390/ijms26167976 - 18 Aug 2025
Abstract
Glioblastoma (GBM) is a highly aggressive brain tumour characterised by a poor prognosis and resistance to anti-angiogenic treatments. Vasculogenic mimicry (VM), in which tumour cells form vessel-like structures independent of endothelial cells, has emerged as a key mechanism hindering the efficacy of anti-angiogenic [...] Read more.
Glioblastoma (GBM) is a highly aggressive brain tumour characterised by a poor prognosis and resistance to anti-angiogenic treatments. Vasculogenic mimicry (VM), in which tumour cells form vessel-like structures independent of endothelial cells, has emerged as a key mechanism hindering the efficacy of anti-angiogenic therapies. Recent research highlights the central role of RNA-binding proteins (RBPs) in regulating VM through diverse post-transcriptional mechanisms, including mRNA decay induction and translational repression. Several oncogenic RBPs, such as HuR and HNRNPs, promote VM and tumour aggressiveness, while others, including RBMS3, act as suppressors of VM. Despite the prominent oncogenic roles of multiple RBPs, RBP-targeting compounds aimed at suppressing VM in GBM have remained at an early stage due to a number of limitations. This review summarises the role of VM in the treatment resistance of GBM, RBP regulation of VM, and the current landscape and future direction of RBP-targeted therapies aimed at overcoming VM-mediated treatment resistance in GBM. Full article
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13 pages, 2345 KiB  
Article
CRY1 Lysine 151 Regulates Circadian Rhythms Through Ubiquitination-Independent Protein Interactions
by Jiawen Peng, Na Liu, Yixuan Ren, Jiahui Wang, Yanxia Jin, Xianping Wang, Weidong Wang and Jicheng Pan
Int. J. Mol. Sci. 2025, 26(16), 7962; https://doi.org/10.3390/ijms26167962 - 18 Aug 2025
Abstract
Mammalian circadian rhythms, governing ~24 h oscillations in behavior, physiology, and hormone levels, are orchestrated by transcriptional–translational feedback loops centered around the core clock protein cryptochrome 1 (CRY1). While CRY1 ubiquitination is known to regulate clock function, the roles of specific ubiquitination sites [...] Read more.
Mammalian circadian rhythms, governing ~24 h oscillations in behavior, physiology, and hormone levels, are orchestrated by transcriptional–translational feedback loops centered around the core clock protein cryptochrome 1 (CRY1). While CRY1 ubiquitination is known to regulate clock function, the roles of specific ubiquitination sites remain unclear. Here, we identify lysine 151 (K151) as a critical residue modulating the circadian period through non-canonical mechanisms. Using site-directed mutagenesis, we generated CRY1-K151Q/R mutants mimicking constitutive deubiquitination. Circadian rescue assays in Cry1/2-deficient cells revealed period shortening (K151Q: −2.25 h; K151R: −1.4 h; n = 3, p < 0.01, Student’s t-test), demonstrating K151’s functional importance. Despite normal nuclear localization kinetics, K151Q/R mutants exhibited reduced transcriptional repression in luciferase assays, a weakened interaction with BMAL1 by the luciferase complementation assay, and enhanced binding to E3 ligase FBXL12 (but not FBXL3) while showing more stability than wild-type CRY1. Notably, the absence of ubiquitination-linked degradation or altered FBXL3 engagement suggests a ubiquitination-independent mechanism. We propose that CRY1-K151 serves as a structural hub fine-tuning circadian periodicity by modulating core clock protein interactions rather than through traditional ubiquitin-mediated turnover. These findings redefine the mechanistic landscape of post-translational clock regulation and offer new therapeutic avenues for circadian disorders. Full article
(This article belongs to the Special Issue The Importance of Molecular Circadian Rhythms in Health and Disease)
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14 pages, 2613 KiB  
Article
miR-7a-5p Contributes to Suppressing NLRP3/Caspase-1 Signaling Pathway in Response to Streptococcus suis Type 2 Infection
by Ziteng Deng, Qian Sun, Shun Li, Yibo Wang, Yuxin Che, Yunfei Huang, Jiedan Liao, Honglin Xie, Xiaoshu Zhan, Qinqin Sun and Qiang Fu
Microorganisms 2025, 13(8), 1924; https://doi.org/10.3390/microorganisms13081924 - 18 Aug 2025
Viewed by 40
Abstract
Streptococcus suis type 2 (SS2) is a pathogen causing diseases like meningitis and septicaemia worldwide. While microRNAs (miRNAs) are acknowledged for their role in post-transcriptional regulation of gene expression and influence on immune responses, their exact functions in hosts during SS2 infection remain [...] Read more.
Streptococcus suis type 2 (SS2) is a pathogen causing diseases like meningitis and septicaemia worldwide. While microRNAs (miRNAs) are acknowledged for their role in post-transcriptional regulation of gene expression and influence on immune responses, their exact functions in hosts during SS2 infection remain elusive. This study aims to explore the role of miR-7a-5p in macrophages during SS2 infection. Our findings reveal that SS2 infection in J774A.1 cells triggers upregulation of the NLRP3 inflammasome signaling pathways, evidenced by enhanced mRNA expression of pro-inflammatory cytokines (IL-6, IL-18, IL-23, TNF-α) and elevated protein levels of NLRP3, caspase-1, and IL-1β. Concurrently, SS2 infection reduces miR-7a-5p expression. Dual-luciferase reporter assays confirm that miR-7a-5p directly targets the 3′UTR of NLRP3 mRNA. Notably, miR-7a-5p overexpression in SS2-infected J774A.1 cells suppresses NLRP3 inflammasome activation and downstream signaling, as demonstrated by reduced mRNA levels of inflammatory mediators and decreased protein levels of NLRP3, caspase-1, IL-1β, and IL-18. Conversely, miR-7a-5p inhibition produces effects opposite to those of overexpression. In mice, administration of miR-7a-5p mimics mitigates SS2-induced lung, liver, and spleen damage, reducing histological scores in these organs. Collectively, these results show that miR-7a-5p alleviates SS2-induced inflammation by inhibiting the NLRP3 inflammasome, underscoring its potential as a therapeutic target for SS2-associated diseases. Full article
(This article belongs to the Section Veterinary Microbiology)
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12 pages, 1707 KiB  
Article
Characteristics of the Insulin-like Peptide Genes and Their Roles in the Ovarian Development of Zeugodacus cucurbitae (Coquillett)
by Jun-Chen Yi, Chuan-Lian Liu, Dong Chen, Dong Wei and Zhu-Ting Zhang
Insects 2025, 16(8), 854; https://doi.org/10.3390/insects16080854 - 17 Aug 2025
Viewed by 146
Abstract
The melon fly Zeugodacus cucurbitae (Coquillett) is a globally invasive pest responsible for substantial economic losses in the fruit and vegetable industries. Insulin-like peptides (ILPs) are evolutionarily conserved neuropeptides that play a crucial role in insect reproduction. In this study, six ZcILPs from [...] Read more.
The melon fly Zeugodacus cucurbitae (Coquillett) is a globally invasive pest responsible for substantial economic losses in the fruit and vegetable industries. Insulin-like peptides (ILPs) are evolutionarily conserved neuropeptides that play a crucial role in insect reproduction. In this study, six ZcILPs from the melon fly, designated as ZcILP16, were cloned. Phylogenetic analysis demonstrated a strong orthologous link with Dipteran ILPs. Spatiotemporal expression profiling revealed that ZcILP1 and ZcILP3 exhibit preferential enrichment in the adult female fat body, with their expression specifically and significantly upregulated in 5-day-old individuals. Their expression decreased 12, 24, and 48 h post-starvation and increased upon re-feeding. Silencing ZcILP1 and ZcILP3 resulted in reduced ovarian size by 51.42% and 69.17%, respectively. Furthermore, silencing ZcILP1 or ZcILP3 significantly decreased the transcriptional levels of genes downstream of the insulin signaling pathway (ISP), notably the target of rapamycin (ZcTOR) and Forkhead box O (ZcFOXO). Concurrently, the expression of Vitellogenin (ZcVg), a gene associated with reproduction, was significantly downregulated. These findings indicate that ZcILP1 and ZcILP3 regulate ZcVgs expression and ovarian development through ISP, suggesting them as potential targets for green control of Z. cucurbitae. Full article
(This article belongs to the Section Insect Physiology, Reproduction and Development)
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18 pages, 6274 KiB  
Article
iTRAQ-Based Phosphoproteomic Profiling Reveals Spermidine Enhanced SOS Signaling and Metabolic Reprogramming in Cucumber Seedlings Under Salt Stress
by Bin Li, Danyi Wang, Liru Ren, Bo Qiao, Lincao Wei and Lingjuan Han
Horticulturae 2025, 11(8), 973; https://doi.org/10.3390/horticulturae11080973 - 17 Aug 2025
Viewed by 203
Abstract
Soil salinity severely impairs plant growth, and polyamines such as spermidine (Spd) are known to bolster stress tolerance by acting as osmoprotectants and signaling molecules. Using TiO2 enrichment, iTRAQ quantification, and bioinformatics analysis, we identified 870 proteins and 157 differentially phosphorylated proteins. [...] Read more.
Soil salinity severely impairs plant growth, and polyamines such as spermidine (Spd) are known to bolster stress tolerance by acting as osmoprotectants and signaling molecules. Using TiO2 enrichment, iTRAQ quantification, and bioinformatics analysis, we identified 870 proteins and 157 differentially phosphorylated proteins. Functional annotation showed that salt stress activated key components of the Salt Overly Sensitive pathway, particularly serine threonine kinases (SOS2) and Ca2+ binding sensors (SOS3). Among thirty-six SOS-associated kinases detected, eight SOS2 isoforms, four MAPKs, and two SOS3 homologs were significantly upregulated by NaCl, and Spd further increased the phosphorylation of six SOS2 proteins and one SOS3 protein under salt stress, with no detectable effect on SOS1. qRT PCR revealed enhanced expression of MAPKs and calcium-dependent protein kinases, suggesting a phosphorylation-centered model in which Spd amplifies Ca2+-mediated SOS signaling and reinforces ion homeostasis through coordinated transcriptional priming and post-translational control. Additional, proteins involved in protein synthesis and turnover (ribosomal subunits, translation initiation factors, ubiquitin–proteasome components), DNA replication and transcription, and RNA processing showed differential expression under salt or Spd treatment. Central metabolic pathways were reprogrammed, involving glycolysis, the TCA cycle, the pentose phosphate pathway, as well as ammonium transporters and amino acid biosynthetic enzymes. These findings indicate that exogenous Spd regulated phosphorylation-mediated networks involving the SOS signaling pathway, protein homeostasis, and metabolism, thereby enhancing cucumber salt tolerance. Full article
(This article belongs to the Section Biotic and Abiotic Stress)
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45 pages, 1602 KiB  
Review
Mechanisms and Genetic Drivers of Resistance of Insect Pests to Insecticides and Approaches to Its Control
by Yahya Al Naggar, Nedal M. Fahmy, Abeer M. Alkhaibari, Rasha K. Al-Akeel, Hend M. Alharbi, Amr Mohamed, Ioannis Eleftherianos, Hesham R. El-Seedi, John P. Giesy and Hattan A. Alharbi
Toxics 2025, 13(8), 681; https://doi.org/10.3390/toxics13080681 - 16 Aug 2025
Viewed by 429
Abstract
The escalating challenge of resistance to insecticides among agricultural and public health pests poses a significant threat to global food security and vector-borne disease control. This review synthesizes current understanding of the molecular mechanisms underpinning resistance, including well-characterized pathways such as target-site mutations [...] Read more.
The escalating challenge of resistance to insecticides among agricultural and public health pests poses a significant threat to global food security and vector-borne disease control. This review synthesizes current understanding of the molecular mechanisms underpinning resistance, including well-characterized pathways such as target-site mutations affecting nicotinic acetylcholine receptors (nAChRs), acetylcholinesterase (AChE), voltage-gated sodium channels (VGSCs), and γ-aminobutyric acid (GABA) receptors, and metabolic detoxification mediated by cytochrome P450 monooxygenases (CYPs), esterases, and glutathione S-transferases (GSTs). Emerging resistance mechanisms are also explored, including protein sequestration by odorant-binding proteins and post-transcriptional regulation via non-coding RNAs, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Focused case studies on Aedes aegypti and Spodoptera frugiperda illustrate the complex interplay of genetic and biochemical adaptations driving resistance. In Ae. aegypti, voltage-gated sodium channel (VGSCs) mutations (V410L, V1016I, F1534C) combined with metabolic enzyme amplification confer resistance to pyrethroids, accompanied by notable fitness costs and ecological impacts on vector populations. In S. frugiperda, multiple resistance mechanisms, including overexpression of cytochrome P450 genes (e.g., CYP6AE43, CYP321A8), target-site mutations in ryanodine receptors (e.g., I4790K), and behavioral avoidance, have rapidly evolved across global populations, undermining the efficacy of diamide, organophosphate, and pyrethroid insecticides. The review further evaluates integrated pest management (IPM) strategies, emphasizing the role of biopesticides, biological control agents, including entomopathogenic fungi and parasitoids, and molecular diagnostics for resistance management. Taken together, this analysis underscores the urgent need for continuous molecular surveillance, the development of resistance-breaking technologies, and the implementation of sustainable, multifaceted interventions to safeguard the long-term efficacy of insecticides in both agricultural and public health contexts. Full article
(This article belongs to the Special Issue Impacts of Agrochemicals on Insects and Soil Organisms)
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18 pages, 511 KiB  
Review
Roles and Prospective Applications of Ferroptosis Suppressor Protein 1 (FSP1) in Malignant Tumor Treatment
by Zhesi Jin, Qian Zhang, Yinlong Pan, Hao Chen, Ke Zhou, Huazhong Cai and Pan Huang
Curr. Oncol. 2025, 32(8), 456; https://doi.org/10.3390/curroncol32080456 - 14 Aug 2025
Viewed by 151
Abstract
Ferroptosis suppressor protein 1 (FSP1) has emerged as a critical regulator of ferroptosis, an iron-dependent form of programmed cell death with significant therapeutic potential in cancer treatment. Despite rapidly expanding research, current knowledge on FSP1 remains fragmented across various tumor types and experimental [...] Read more.
Ferroptosis suppressor protein 1 (FSP1) has emerged as a critical regulator of ferroptosis, an iron-dependent form of programmed cell death with significant therapeutic potential in cancer treatment. Despite rapidly expanding research, current knowledge on FSP1 remains fragmented across various tumor types and experimental contexts. The aim of this review is to systematically integrate the latest evidence regarding the molecular structure, biological functions, and regulatory mechanisms controlling FSP1 expression, emphasizing its involvement in tumor progression and resistance to therapy. Readers can expect comprehensive coverage of FSP1’s structural characteristics, enzymatic roles, transcriptional and post-transcriptional regulation, and its pathological significance in hepatocellular carcinoma, colorectal cancer, pancreatic cancer, gastric cancer, breast cancer, lung cancer, and leukemia. We further evaluate emerging therapeutic strategies targeting FSP1 aimed at overcoming resistance and improving clinical outcomes. Relevant studies were systematically identified by searching PubMed, Web of Science, and Embase databases, focusing particularly on the recent and impactful literature to guide future research directions. Full article
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20 pages, 4584 KiB  
Article
Systemic Lonp1 Haploinsufficiency Mitigates Cardiac Mitochondrial Dysfunction Induced by Cardiomyocyte-Specific Lonp1 Haploinsufficiency via Potential Inter-Organ Crosstalk
by Sakthijothi Muthu, Zinnia Tran, Ramasamy Saminathan, Pratikshya Shrestha and Sundararajan Venkatesh
Biomolecules 2025, 15(8), 1159; https://doi.org/10.3390/biom15081159 - 13 Aug 2025
Viewed by 303
Abstract
Efficient mitochondrial matrix protein quality control (mPQC), regulated by the mitochondrial matrix protease LONP1, is essential for preserving cardiac bioenergetics, particularly in post-mitotic cardiomyocytes, which are highly susceptible to mitochondrial dysfunction. While cardiac mPQC defects could impair heart function, it remains unclear whether [...] Read more.
Efficient mitochondrial matrix protein quality control (mPQC), regulated by the mitochondrial matrix protease LONP1, is essential for preserving cardiac bioenergetics, particularly in post-mitotic cardiomyocytes, which are highly susceptible to mitochondrial dysfunction. While cardiac mPQC defects could impair heart function, it remains unclear whether such defects can be mitigated through inter-organ crosstalk by modulating mPQC in extra-cardiac tissues, a potentially valuable strategy given the challenges of directly targeting the heart. To investigate this, we examined two mouse models of Lonp1 haploinsufficiency at young adulthood: a cardiomyocyte-specific heterozygous knockout (Lonp1CKO-HET) and a whole-body heterozygous knockout (Lonp1GKO-HET). Despite similar reductions in Lonp1 mRNA expression in the hearts, Lonp1GKO-HET mice exhibited no cardiac dysfunction, whereas Lonp1CKO-HET mice showed mild cardiac dysfunction accompanied by activation of the mitochondrial stress response, including induction of genes such as Clpx, Spg7, Hspa9, and Hspd1, increased mitochondrial dynamics (Pink1, Dnm1l), reduced mitochondrial biogenesis, and compensatory upregulation of the mtDNA transcriptional regulator Tfam, all occurring without overt structural remodeling. These alterations were absent in Lonp1GKO-HET hearts. Our findings reveal a novel adaptive mechanism in which systemic mPQC deficiency can buffer mitochondrial dysfunction in the heart through inter-organ communication that is lost with cardiomyocyte-specific mPQC disruption. This study identifies systemic modulation of Lonp1-mediated mitochondrial stress pathways as a promising strategy to promote cardiac resilience through protective inter-organ signaling. Full article
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17 pages, 1940 KiB  
Review
Plant Long Non-Coding RNAs: Multilevel Regulators of Development, Stress Adaptation, and Crop Improvement
by Xiyue Bao, Xiaofeng Dai, Jieyin Chen and Ran Li
Agronomy 2025, 15(8), 1950; https://doi.org/10.3390/agronomy15081950 - 13 Aug 2025
Viewed by 264
Abstract
Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of various biological processes in plants, including development, stress responses, and pathogen defense. Advances in multi-omics sequencing analysis and molecular biology methods have significantly expanded our understanding of the plant lncRNA landscape, revealing novel [...] Read more.
Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of various biological processes in plants, including development, stress responses, and pathogen defense. Advances in multi-omics sequencing analysis and molecular biology methods have significantly expanded our understanding of the plant lncRNA landscape, revealing novel lncRNAs across diverse species. In this review, we provided an overview of the essential roles of lncRNAs in multilevel regulatory functions in plant growth, development, and stress responses. Moreover, we bridged the module network among these different conditions. One of the most important functions of lncRNA is gene expression regulation. Thus, we summarized the plant lncRNAs acting in cis/trans and as endogenous target mimics (eTMs) to influence the expression of target genes in transcription and post-transcription regulation. This review also sheds light on several application values in agricultural production and development of plant-specific databases and bioinformatic tools. These datasets facilitated the exploration of lncRNA function, enabling the identification of their expression patterns, phylogenetic relationships, and molecular interactions. As research progresses, multi-omics approaches will provide deeper insights into the regulatory mechanisms of lncRNAs, offering promising strategies for enhancing crop resilience and productivity in response to climate change. Full article
(This article belongs to the Section Crop Breeding and Genetics)
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25 pages, 1455 KiB  
Article
Expression Analysis of miR-519a-3p and miR-379-5p in Colorectal Cancer Patients: A Combined Experimental and Bioinformatic Approach
by Turkan Gurer, Mehmet Emin Kizakoglu, Alper Aytekin and Rusen Avsar
Diagnostics 2025, 15(16), 2023; https://doi.org/10.3390/diagnostics15162023 - 13 Aug 2025
Viewed by 301
Abstract
Background/Objectives: Colorectal cancer (CRC) is one of the most common malignancies worldwide. microRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression post-transcriptionally and have emerged as important regulators in cancer biology. This study aimed to investigate the roles of miR-379-5p and [...] Read more.
Background/Objectives: Colorectal cancer (CRC) is one of the most common malignancies worldwide. microRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression post-transcriptionally and have emerged as important regulators in cancer biology. This study aimed to investigate the roles of miR-379-5p and miR-519a-3p in CRC using Quantitative Real-Time PCR (RT-qPCR) and comprehensive bioinformatic analyses. Methods: Tumor tissues and matched adjacent normal tissues were collected from 54 patients with CRC. The expression levels of miR-379-5p and miR-519a-3p in these tissues were determined using the RT-qPCR method. To investigate the functional roles of differently expressed miRNAs, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to construct miRNA–transcription factor (TF)–target gene–disease interaction networks. Results: It was found that the expression level of miR-379-5p was statistically significantly increased in tumor tissues compared to normal tissues, while miR-519a-3p was decreased (p < 0.05). GO analysis revealed enrichment in several important biological processes, including cellular protein metabolic processes, biosynthetic processes, response to stress, and nucleic acid binding TF activity. KEGG analysis exhibited that dysregulated miRNAs were associated with important pathways related to carcinogenesis, such as p53 signaling, TGF-beta signaling, and FoxO signaling pathways. Additionally, the miRNAs-TFs-Genes-Diseases Networks analysis identified ESR1 and FOXA1 as common target TFs of dysregulated miRNAs. Network analyses showed that dysregulated miRNAs interact with CRC-associated genes (Caspase 3 (CASP3), Adenomatous polyposis coli (APC), and AKT serine/threonine kinase 3 (AKT3)). Conclusions: The present study indicates that miR-379-5p and miR-519a-3p may be involved in CRC progression, with miR-379-5p being upregulated and miR-519a-3p being downregulated in tumor tissues. However, further functional studies are required to clarify their potential roles in tumor biology. The findings of the study suggest that miR-379-5p and miR-519a-3p may be associated with regulatory pathways related to CRC. These miRNAs have the potential to serve as diagnostic biomarkers or therapeutic targets in CRC. Full article
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14 pages, 1820 KiB  
Review
Approaches for Identifying LncRNA-Associated Proteins for Therapeutic Targets and Cancer Biomarker Discovery
by Mohammad Shabir Hussain, Puneet Vij, Sudhir Kotnala, Shadab Ahmad, Subhash C. Chauhan and Manish K. Tripathi
Targets 2025, 3(3), 27; https://doi.org/10.3390/targets3030027 - 11 Aug 2025
Viewed by 237
Abstract
Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators of gene expression and cellular signaling in cancer. Their functions are primarily mediated through interactions with specific protein partners that modulate chromatin structure, epigenetic remodeling, transcription, and signal transduction. In this review, we [...] Read more.
Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators of gene expression and cellular signaling in cancer. Their functions are primarily mediated through interactions with specific protein partners that modulate chromatin structure, epigenetic remodeling, transcription, and signal transduction. In this review, we explore reports and strategies for the proteomic characterization of lncRNA-associated proteins, particularly emphasizing high-throughput liquid chromatography–mass spectrometry (LC-MS)-based techniques. Affinity-based methods such as RNA pull-down, ChIRP MS, RAP-MS, BioID-MS, and SILAC-MS enable sensitive and specific mapping of lncRNA and protein complexes. These approaches reveal cancer-specific proteomic signatures, post-translational modifications, and mechanistic insights into tumor biology. The use of label-free quantification, bituminization, and crosslinking strategies further enhances the resolution of dynamic RNA–protein networks. Validation tools following bioinformatic analyses, such as Western blotting, immunohistochemistry, immunofluorescence, and ELISA, are used to prioritize and confirm findings. Candidate biomarkers from hepatocellular carcinoma to colorectal and prostate cancers, profiling lncRNA-associated proteins, hold promise for identifying clinically actionable biomarkers and therapeutic targets. This review highlights the translational relevance of lncRNA protein studies and advocates for their broader adoption in oncological research. In LC-MS workflows, proteins bound to lncRNAs are enzymatically digested into peptides, separated via nano-LC, and analyzed using high-resolution tandem MS. Label-free or isotope-labeled methods quantify differential enrichment, followed by bioinformatics-driven pathway annotation. Full article
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25 pages, 12359 KiB  
Review
Metabolism in Sync: The Circadian Clock, a Central Hub for Light-Driven Chloroplastic and Mitochondrial Entrainment
by Luis Cervela-Cardona, Marta Francisco and Åsa Strand
Plants 2025, 14(16), 2464; https://doi.org/10.3390/plants14162464 - 8 Aug 2025
Viewed by 511
Abstract
Plants align their physiology with daily environmental cycles through the circadian clock, which integrates light and metabolic signals to optimize growth and stress responses. While light entrainment has been extensively studied, emerging evidence highlights the central role of metabolism—particularly from chloroplasts and mitochondria—in [...] Read more.
Plants align their physiology with daily environmental cycles through the circadian clock, which integrates light and metabolic signals to optimize growth and stress responses. While light entrainment has been extensively studied, emerging evidence highlights the central role of metabolism—particularly from chloroplasts and mitochondria—in tuning circadian rhythms. In this review, we explore the bidirectional relationship between organelle metabolism and the circadian clock, focusing on how metabolic signals such as sugars, ROS, and organic acids function as entrainment cues. We discuss how the clock regulates organelle function at multiple levels, including transcriptional, translational, and post-translational mechanisms, and how organelle-derived signals feedback to modulate core clock components through retrograde pathways. Special attention is given to the integration of chloroplast and mitochondrial signals, emphasizing their synergistic roles in maintaining cellular homeostasis. Drawing on the “three-body problem” analogy, we illustrate the dynamic and reciprocal interactions among light, clock, and metabolism. This perspective underscores the need to reframe the circadian system, not merely as light-driven but also as a central integrator of energy status and environmental cues. Understanding this integrated network is essential to improve plant performance and resilience under fluctuating environmental conditions. Full article
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17 pages, 5338 KiB  
Article
Plasma Biomarkers of Mitochondrial Dysfunction in Patients with Myasthenia Gravis
by Elena E. Timechko, Marina I. Severina, Alexey M. Yakimov, Anastasia A. Vasilieva, Anastasia I. Paramonova, Natalya V. Isaeva, Semen V. Prokopenko and Diana V. Dmitrenko
Med. Sci. 2025, 13(3), 118; https://doi.org/10.3390/medsci13030118 - 8 Aug 2025
Viewed by 212
Abstract
Background. Myasthenia gravis is an autoimmune neuromuscular disease characterized by fatigue of striated muscles due to impaired neuromuscular transmission. Mitochondrial dysfunction, according to published data, contributes significantly to metabolic abnormalities, oxidative stress and, as a consequence, the persistence of inflammation. MicroRNAs, which [...] Read more.
Background. Myasthenia gravis is an autoimmune neuromuscular disease characterized by fatigue of striated muscles due to impaired neuromuscular transmission. Mitochondrial dysfunction, according to published data, contributes significantly to metabolic abnormalities, oxidative stress and, as a consequence, the persistence of inflammation. MicroRNAs, which are post-transcriptional regulators of expression, are able to contribute to the aberrant functioning of mitochondria. In this study, with the aim of searching for biomarkers at the level of circulating microRNAs and proteins, the expression of three microRNAs was analyzed and the concentration of mitochondrial proteins was measured in the blood plasma of patients with myasthenia gravis (n = 49) in comparison with healthy volunteers (n = 31). Methods. Expression analysis was performed by RT-PCR, mathematical data processing was carried out using the Livak method, and protein concentration was determined by enzyme immunoassay. Results. Our plasma expression analysis revealed a statistically significant increase in hsa-miR-194-5p expression (Log10 Fold Change = 1.46, p-value < 0.0001) and a statistically significant decrease in hsa-miR-148a-3p expression (Log10 Fold Change = −0.65, p-value = 0.02). A statistically significant decrease in plasma COQ10A concentration was also found (0.911 [0.439; 1.608] versus 1.815 [1.033; 2.916] for myasthenia gravis and controls, respectively, p-value = 0.01). Conclusion. Our data suggest hsa-miR-148a-3p and hsa-miR-194-5p, as well as COQ10A, as potential biomarkers of mitochondrial dysfunction in myasthenia gravis. Full article
(This article belongs to the Section Neurosciences)
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