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Open AccessArticle

Anticancer Activity of 2,3′-Dihydroxy-5′-Methoxystilbene Against NSCLC Cell Lines Through AKT-Dependent Mechanisms: A Comprehensive In Vitro and Computational Analysis

by Phisit Pouyfung, Nonthalert Lertnitikul, Noriyoshi Ogino, Achitphol Chookaew, Varisa Pongrakhananon, Piriya Chonsut, Natthaporn Sueangoen and Suwichak Chaisit

Int. J. Mol. Sci. 2026, 27(2), 719; https://doi.org/10.3390/ijms27020719 - 10 Jan 2026

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Abstract

Lung cancer remains a major clinical challenge, with therapy resistance in non-small-cell lung cancer (NSCLC) driving the search for novel selective agents. This study demonstrates that 2,3′-dihydroxy-5′-methoxystilbene exhibits significant anticancer activity in NSCLC cell lines (A549, H23, and H460) while displaying substantially lower [...] Read more.

Lung cancer remains a major clinical challenge, with therapy resistance in non-small-cell lung cancer (NSCLC) driving the search for novel selective agents. This study demonstrates that 2,3′-dihydroxy-5′-methoxystilbene exhibits significant anticancer activity in NSCLC cell lines (A549, H23, and H460) while displaying substantially lower toxicity toward normal NIH/3T3 fibroblasts. The compound reduced the viability of H23 and H460 cells after 48 h. (IC50: 23.39 ± 3.27 μM and 24.20 ± 2.61 μM, respectively), with NIH/3T3 cells remaining comparatively resistant (IC50 > 100 μM). At 25 μM, it suppressed proliferation by approximately 40% in H23, 30% in H460, and 20% in A549 cells, and dose-dependently impaired colony formation and migration, leading to near-complete migration arrest in H460 cells. Apoptosis induction peaked at 19% in H23, 17% in H460, and 8% in A549 cells at 25 μM. Mechanistic studies and molecular modeling revealed AKT-dependent activity, with decreased p-AKT and p-GSK3β levels (0.70 and 0.75 in H23; 0.65 and 0.70 in H460 at 25 μM), without changes in total protein expression. Combination treatment with cisplatin yielded synergistic effects in A549 (CI = 0.83) and H460 (CI = 0.94) cells, but antagonistic effects in H23 cells (CI = 1.32). These findings identify 2,3′-dihydroxy-5′-methoxystilbene as a selective AKT-targeting stilbene with promising anticancer potential and context-dependent chemosensitizing activity in NSCLC cells. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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18 pages, 4597 KB

Open AccessArticle

A Combined Bioinformatics and Clinical Validation Study Identifies MDM2, FKBP5 and CTNNA1 as Diagnostic Gene Signatures for COPD in Peripheral Blood Mononuclear Cells

by Innokenty A. Savin, Aleksandra V. Sen’kova, Andrey V. Markov, Olga S. Kotova, Ilya S. Shpagin, Lyubov A. Shpagina, Valentin V. Vlassov and Marina A. Zenkova

Int. J. Mol. Sci. 2026, 27(1), 273; https://doi.org/10.3390/ijms27010273 - 26 Dec 2025

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Abstract

Chronic obstructive pulmonary disease (COPD) is often diagnosed after significant lung damage has already occurred, highlighting a need for minimally invasive biomarkers for early detection of COPD development. This study aims to identify transcriptional biomarkers in peripheral blood mononuclear cells (PBMCs). A Weighted [...] Read more.

Chronic obstructive pulmonary disease (COPD) is often diagnosed after significant lung damage has already occurred, highlighting a need for minimally invasive biomarkers for early detection of COPD development. This study aims to identify transcriptional biomarkers in peripheral blood mononuclear cells (PBMCs). A Weighted Gene Co-Expression Network Analysis (WGCNA) was performed on the GSE146560 transcriptomic dataset. Hub genes were cross-validated using independent transcriptomic data (GSE94916), topology analysis of a COPD-related protein–protein interaction (PPI) network, and a text-mining approach. The top candidate genes were validated using RT-qPCR in a clinical cohort, consisting of 28 COPD patients and 13 healthy volunteers, and their diagnostic value was evaluated using receiver operating characteristic (ROC) analysis. WGCNA identified four gene modules significantly correlated with COPD, the functional annotation of which revealed their enrichment in immune and tissue remodeling pathways. Further analysis of the PPI network topology structure and gene expression revealed a hub gene signature that was significantly upregulated in PBMCs of COPD patients, including MDM2 (6.3-fold, p < 0.001), FKBP5 (7.0-fold, p < 0.001), and CTNNA1 (10.0-fold, p < 0.001). ROC analysis demonstrated high diagnostic accuracy for these genes, with AUC values of 0.849, p < 0.001, for MDM2, 0.957, p < 0.001, for FKBP5, and 0.958, p < 0.001, for CTNNA1. MDM2, FKBP5, and CTNNA1 represent promising, readily accessible PBMC biomarkers for COPD diagnosis. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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14 pages, 2156 KB

Open AccessArticle

Effect of Soluble Factors Released from Porcine Freeze-Dried Lung Tissue (FDLT) on Modulation of Cell Growth and EMT Signature in Non-Small Cell Lung Cancer (NSCLC)—A Preliminary In Vitro Study

by Umme Samia, Daniela Omodei, Luisa Amato, Caterina De Rosa, Rosa Camerlingo, Virna Conti, Stefano Grolli, Orlando Ferroni, Adriano Piattelli, Giovanni N. Roviello, Carminia Maria Della Corte, Viviana De Rosa, Maria Cristina Curia and Francesca Iommelli

Int. J. Mol. Sci. 2025, 26(23), 11743; https://doi.org/10.3390/ijms262311743 - 4 Dec 2025

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Abstract

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with therapeutic efficacy often hindered by the development of multidrug resistance. Consequently, alternative strategies to slow down tumor progression warrant rigorous investigation. Bioactive molecules derived from tissues and organs have shown [...] Read more.

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with therapeutic efficacy often hindered by the development of multidrug resistance. Consequently, alternative strategies to slow down tumor progression warrant rigorous investigation. Bioactive molecules derived from tissues and organs have shown potential therapeutic properties for several diseases. We investigated the biological role of soluble bioactive factors derived from lyophilized porcine freeze-dried lung tissue (FDLT), as they may contain tumor-suppressing components involved in the progression of non-small cell lung cancer (NSCLC). NSCLC H1975 and PC9 cell lines were treated with FDLT at concentrations of 0.25 mg/mL and 0.5 mg/mL. Cell cycle analysis and mitochondrial membrane potential (MMP) assays were performed to assess cell proliferation and cell death activation. In parallel, epithelial–mesenchymal transition (EMT) markers were detected by qRT-PCR. Our findings showed that FDLT treatment reduced the viability of H1975 and PC9 cells in a dose-dependent manner, along with significant suppression of cell proliferation and colony formation. Moreover, FDLT treatment altered the cell cycle phases and determined a concomitant reduction of cyclin D1 levels as well as induction of mitochondria depolarization by suppressing MMP. Finally, qRT-PCR revealed significant downregulation of EMT-related genes vimentin and N-cadherin, along with the EMT transcription factor Twist. These findings highlight soluble FDLT-derived biomolecules as a potential tool to design alternative treatment strategies for NSCLC. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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13 pages, 1545 KB

Open AccessArticle

Hematological Biomarkers for Early Detection of Lung Cancer: Evaluating the Diagnostic Potential of Circulating Interleukin Levels

by Ouafaa Morjani, Yi-Wei Yang, Rachid Lahlil, Hamid Lakhiari and Hassan Alaoui

Int. J. Mol. Sci. 2025, 26(22), 11014; https://doi.org/10.3390/ijms262211014 - 14 Nov 2025

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Abstract

Early detection of lung cancer remains a major unmet clinical need, as most patients are diagnosed at advanced stages when curative treatment options are limited. Circulating cytokines and interleukins represent promising molecular biomarkers for the non-invasive diagnosis and monitoring of tumor development. In [...] Read more.

Early detection of lung cancer remains a major unmet clinical need, as most patients are diagnosed at advanced stages when curative treatment options are limited. Circulating cytokines and interleukins represent promising molecular biomarkers for the non-invasive diagnosis and monitoring of tumor development. In this study, we investigated the diagnostic potential of plasma interleukins in distinguishing early-stage non-small cell lung cancer (NSCLC) from healthy individuals and patients with chronic obstructive pulmonary disease (COPD). Quantitative analyses demonstrated significantly elevated plasma levels of IL-1RA, IL-6, IL-8, IL-10, and IL-17A in NSCLC patients compared with healthy controls. Among these, a composite biomarker panel comprising IL-6, IL-10, IL-8, and IL-1RA exhibited the highest diagnostic performance, outperforming individual cytokines and other combinations. This interleukin-based signature also differentiated NSCLC from COPD with strong specificity, underscoring its potential clinical applicability. These findings highlight the molecular and translational relevance of plasma interleukin profiling as a non-invasive diagnostic approach for early lung cancer detection, potentially enabling earlier intervention and improved patient outcomes. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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41 pages, 11700 KB

Open AccessArticle

Effect of Reoxygenation on Radioresistance of Chronically Hypoxic A549 Non-Small Cell Lung Cancer (NSCLC) Cells Following X-Ray and Carbon Ion Exposure

by Hasan Nisar, Bikash Konda, Marie Denise Hoffmann, Frederik M. Labonté, Maryam Arif, Sebastian Diegeler, Claudia Schmitz, Christa Baumstark-Khan, François Chevalier and Christine E. Hellweg

Int. J. Mol. Sci. 2025, 26(18), 9153; https://doi.org/10.3390/ijms26189153 - 19 Sep 2025

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Abstract

Hypoxia-induced radioresistance in non-small cell lung cancer (NSCLC) hinders radiotherapy efficacy. Fractionated schedules exploit reoxygenation between fractions to reverse this resistance, but the effects of post-irradiation reoxygenation remain unclear and may depend on radiation quality. We investigated survival, cell cycle progression, cytokine secretion, [...] Read more.

Hypoxia-induced radioresistance in non-small cell lung cancer (NSCLC) hinders radiotherapy efficacy. Fractionated schedules exploit reoxygenation between fractions to reverse this resistance, but the effects of post-irradiation reoxygenation remain unclear and may depend on radiation quality. We investigated survival, cell cycle progression, cytokine secretion, and gene expression in hypoxic (1 % O₂) and reoxygenated A549 cells irradiated with X-rays or carbon ions. Colony-forming assays revealed an Oxygen Enhancement Ratio (OER) > 1 for both hypoxic and reoxygenated cells after X-rays, indicating persistent radioresistance; carbon ion OER ≈ 1 reflected oxygen-independent cytotoxicity. Hypoxia weakened radiation-induced G₂ arrest, and this was unaffected by reoxygenation. IL-6 secretion increased after X-rays and IL-8 after carbon ions exposure; both were enhanced under hypoxia and reoxygenation. RNA sequencing revealed that hypoxia induced a pro-survival, epithelial-to-mesenchymal transition (EMT)-promoting, and immune-evasive transcriptional program, which was largely reversed by reoxygenation but without increased clonogenic killing. These findings indicate that short-term reoxygenation after irradiation can normalize hypoxia-driven transcriptional changes yet does not restore radiosensitivity, supporting the advantage of high-linear energy transfer (LET) carbon ions for targeting resistant hypoxic NSCLC cells. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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13 pages, 1871 KB

Open AccessArticle

Liquiritin Suppresses Intracellular and Secreted MUC5AC and MUC5B in Human Airway Epithelial Cells

by Ryoma Yoshio and Jun Iwashita

Int. J. Mol. Sci. 2025, 26(16), 8076; https://doi.org/10.3390/ijms26168076 - 21 Aug 2025

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Abstract

The human airway surface is covered by a mucus layer composed primarily of the mucins MUC5AC and MUC5B. Excessive mucin production and secretion by airway epithelial cells in patients with asthma result in airway obstruction and worsened asthma symptoms. This study investigated the [...] Read more.

The human airway surface is covered by a mucus layer composed primarily of the mucins MUC5AC and MUC5B. Excessive mucin production and secretion by airway epithelial cells in patients with asthma result in airway obstruction and worsened asthma symptoms. This study investigated the effects of liquiritin, a widely used flavonoid, on intracellular and secreted MUC5AC and MUC5B levels in the NCI-H292 human airway epithelial cell line. Liquiritin treatment suppressed both mucin types in a dose-dependent manner, accompanied by decreased activity of extracellular signal-regulated kinase (ERK) and p38. The effect of liquiritin was further examined in cells stimulated with phorbol 12-myristate 13-acetate (PMA) to induce excessive mucin production and secretion. Liquiritin dose-dependently reduced PMA-induced increases in intracellular and secreted MUC5AC and MUC5B levels as well as PMA-induced ERK and p38 activity. Overall, these results suggest that liquiritin reduces intracellular and secreted MUC5AC and MUC5B levels by suppressing the ERK and/or p38 signaling pathway. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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22 pages, 6303 KB

Open AccessArticle

A Novel Regulatory Role for RPS4Y1 in Inflammatory and Fibrotic Processes

by Karosham D. Reddy, Senani N. H. Rathnayake, Sobia Idrees, Fia Boedijono, Dikaia Xenaki, Matthew P. Padula, Maarten van den Berge, Alen Faiz and Brian G. G. Oliver

Int. J. Mol. Sci. 2025, 26(13), 6213; https://doi.org/10.3390/ijms26136213 - 27 Jun 2025

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Abstract

Asthma is a chronic inflammatory respiratory disease well-known to demonstrate sexual dimorphism in incidence and severity, although the mechanisms causing these differences remain incompletely understood. RPS4X and RPS4Y1 are X and Y-chromosome-linked genes coding ribosomal subunits previously associated with inflammation, airway remodelling and [...] Read more.

Asthma is a chronic inflammatory respiratory disease well-known to demonstrate sexual dimorphism in incidence and severity, although the mechanisms causing these differences remain incompletely understood. RPS4X and RPS4Y1 are X and Y-chromosome-linked genes coding ribosomal subunits previously associated with inflammation, airway remodelling and asthma medication efficacy. Particularly, RPS4Y1 has been under-investigated within the context of disease, with little examination of molecular mechanisms and pathways regulated by this gene. The ribosome, a vital cellular machinery, facilitates the translation of mRNA into peptides and then proteins. Imbalance or dysfunction in ribosomal components may lead to malfunctioning proteins. Using CRISPR-Cas9 knockout cellular models for RPS4Y1 and RPS4X, we characterised the function of RPS4Y1 in the context of the asthma-relevant processes, inflammation and fibrosis. No viable RPS4X knockouts could be generated. We highlight novel molecular mechanisms such as specific translation of IL6 and tenascin-C mRNA by RPS4Y1 containing ribosomes. Furthermore, an RPS4Y1-centric gene signature correlates with clinical lung function measurements, specifically in adult male asthma patients. These findings inform the current understanding of sex differences in asthma, as females do not produce the RPS4Y1 protein. Therefore, the pathologically relevant functions of RPS4Y1 may contribute to the complex sexually dimorphic pattern of asthma susceptibility and progression. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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16 pages, 2718 KB

Open AccessArticle

TGF-β Induced by Allergic Lung Inflammation Enhances Os-Teosarcoma Lung Metastasis in a Mouse Comorbidity Model

by Marco J. Sanchez-Rojas, Belen Tirado-Rodriguez, Gabriela Antonio-Andres, Giovanny Soca-Chafre, Daniel D. Hernandez-Cueto, Cesar O. Martinez-Calderon, Mayra Montecillo-Aguado, Juan C. Hernandez-Guerrero, Marco A. Duran-Padilla, Rogelio Hernandez-Pando and Sara Huerta-Yepez

Int. J. Mol. Sci. 2025, 26(11), 5073; https://doi.org/10.3390/ijms26115073 - 24 May 2025

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TGF-β is a central mediator of pulmonary allergic inflammation recently associated with lung metastasis of osteosarcoma. Given the controversial links between cancer and allergic diseases, this study aimed to evaluate the effects of allergic airway inflammation—particularly TGF-β—on osteosarcoma lung metastasis using a comorbidity [...] Read more.

TGF-β is a central mediator of pulmonary allergic inflammation recently associated with lung metastasis of osteosarcoma. Given the controversial links between cancer and allergic diseases, this study aimed to evaluate the effects of allergic airway inflammation—particularly TGF-β—on osteosarcoma lung metastasis using a comorbidity mouse model. Osteosarcoma cells were implanted in BALB/c mice with induced allergic airway inflammation. Lung metastasis was quantified, while PCNA/TGF-β expression was assessed by immunohistochemistry and digital pathology. Bioinformatic analyses of patient datasets compared TGF-β and PCNA expression in metastatic vs. normal tissues, and their association with survival. Mice with allergic inflammation showed increased lung metastases associated with TGF-β production. In patient samples, both TGF-β and PCNA were upregulated in metastatic tissues and correlated with poor overall survival. PCNA was also linked to genes involved in cell proliferation, DNA replication, and repair. Our results show an association between allergic airway inflammation and extensive lung metastasis of osteosarcoma in a comorbidity mouse model with elevated expression of TGF-β and PCNA. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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18 pages, 13833 KB

Open AccessArticle

Host Serine Proteases and Antiviral Innate Immunity as Potential Therapeutic Targets in Influenza A Virus Infection-Induced COPD Exacerbations

by Haiqing Bai, Melissa Rodas, Longlong Si, Yuncheng Man, Jie Ji, Roberto Plebani, Johnathan D. Mercer, Rani K. Powers, Chaitra Belgur, Amanda Jiang, Sean R. R. Hall, Rachelle Prantil-Baun and Donald E. Ingber

Int. J. Mol. Sci. 2025, 26(6), 2549; https://doi.org/10.3390/ijms26062549 - 12 Mar 2025

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Abstract

Lung manifestations of chronic obstructive pulmonary disease (COPD) are often exacerbated by influenza A virus infections; however, the underlying mechanisms remain largely unknown, and hence therapeutic options are limited. Using a physiologically relevant human lung airway-on-a-chip (Airway Chip) microfluidic culture model lined with [...] Read more.

Lung manifestations of chronic obstructive pulmonary disease (COPD) are often exacerbated by influenza A virus infections; however, the underlying mechanisms remain largely unknown, and hence therapeutic options are limited. Using a physiologically relevant human lung airway-on-a-chip (Airway Chip) microfluidic culture model lined with human airway epithelium from COPD or healthy donors interfaced with pulmonary microvascular endothelium, we observed that Airway Chips lined with COPD epithelium exhibit an increased sensitivity to influenza virus infection, as is observed clinically in COPD patients. Differentiated COPD airway epithelial cells display increased inflammatory cytokine production, barrier function loss, and mucus accumulation upon virus infection. Transcriptomic analysis revealed gene expression profiles characterized by upregulation of serine proteases that may facilitate viral entry and downregulation of interferon-related genes associated with antiviral immune responses. Importantly, treatment of influenza virus-infected COPD epithelium with a protease inhibitor, nafamostat, ameliorated the disease phenotype, as evidenced by dampened viral replication, reduced mucus accumulation, and improved tissue barrier integrity. These findings suggest that targeting host serine proteases may represent a promising therapeutic avenue against influenza-afflicted COPD exacerbations. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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Review

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23 pages, 1039 KB

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Blood-Based miRNA Panels for Timely Detection of Non-Small-Cell Lung Cancer: From Biomarker Discovery to Clinical Translation

by Yazan Zedan, Maria Yurievna Konoshenko, Olga Evgenievna Bryzgunova, Antonina Aleksandrovna Ilyushchenko, Yaroslava Mikhailovna Danilova, Stanislav Dmitrievich Gorbunkov, Kirill Alekseevich Zykov and Pavel Petrovich Laktionov

Int. J. Mol. Sci. 2025, 26(24), 12035; https://doi.org/10.3390/ijms262412035 - 14 Dec 2025

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Abstract

Lung cancer (LC) remains a leading cause of global cancer mortality, driving the need for novel timely detection strategies, i.e., stages I–II detection when tumor curation is efficient. Circulating microRNA (miRNAs), with their unique stability in biofluids, offer a powerful approach for non-invasive [...] Read more.

Lung cancer (LC) remains a leading cause of global cancer mortality, driving the need for novel timely detection strategies, i.e., stages I–II detection when tumor curation is efficient. Circulating microRNA (miRNAs), with their unique stability in biofluids, offer a powerful approach for non-invasive detection. This review compiles validated miRNAs implicated in the early stages of non-small-cell lung cancer (NSCLC), elucidating their roles in key oncogenic pathways such as epithelial-mesenchymal transition (EMT), PI3K/AKT/mTOR, and JAK-STAT, which regulate proliferation, apoptosis, and metastasis. Furthermore, we critically evaluate developed miRNA panels with a specific focus on advanced quantification and normalization strategies, including exogenous spike-in controls and data-driven methods like pairwise normalization, to enhance diagnostic accuracy. Consequently, we identify and rank the most viable miRNA candidates according to key analytical and clinical metrics, providing a clear roadmap for translating these biomarkers into effective panels for the timely detection of NSCLC. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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34 pages, 2493 KB

Open AccessReview

Directions of Immunotherapy for Non-Small-Cell Lung Cancer Treatment: Past, Present and Possible Future

by Gian Marco Leone, Grazia Scuderi, Paolo Fagone and Katia Mangano

Int. J. Mol. Sci. 2025, 26(22), 11055; https://doi.org/10.3390/ijms262211055 - 15 Nov 2025

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Abstract

Lung cancer (LC) is one of the most common malignancies and the leading cause of death worldwide. LC is classified into two main histological subtypes: non-small-cell lung cancer (NSCLC), representing the 85% of all LC types, and small-cell lung cancer (SCLC), representing 15% [...] Read more.

Lung cancer (LC) is one of the most common malignancies and the leading cause of death worldwide. LC is classified into two main histological subtypes: non-small-cell lung cancer (NSCLC), representing the 85% of all LC types, and small-cell lung cancer (SCLC), representing 15% of all lung neoplasm. The recent discovery and clinical approval of new therapeutic approaches has resulted in significant advancements in the management of NSCLC patients. This review aims to summarize the current and ongoing clinical trials that have led to the approval of immune checkpoint inhibitors (ICIs) and the emerging immunotherapy approaches for advanced NSCLC patients. Additionally, the current benefits and drawbacks of these therapeutic strategies will be explored. The treatment for NSCLC is evolving toward a more comprehensive approach that considers both the tumor immune history and genomic features. In this respect, we hope that the ongoing research will make it possible to treat each NSCLC patient individually in the near future. Full article

(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)

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