Current molecular medicine最新文献

{"title":"M1 Macrophage-Derived TNF-α Promotes Pancreatic Cancer Ferroptosis Via p38 MAPK-ACSL4 Pathway.","authors":"Ji-Cheng Zhang, Han-Lin Yin, Qiang-da Chen, Guo-Chao Zhao, Ning Pu, Wen-Hui Lou, Wen-Chuan Wu","doi":"10.2174/0115665240374551250630075409","DOIUrl":"https://doi.org/10.2174/0115665240374551250630075409","url":null,"abstract":"<p><p><p>Introduction: Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most malignant gastrointestinal tumors. M1 macrophage, a subtype within the Tumor Microenvironment (TME), plays a vital role in the development of cancer. Despite its anti-tumoral functions, the specific mechanisms of its action remain incompletely understood. </p><p> Methods: The effect of M1 macrophages on the proliferation ability and cell viability of PDAC cells was evaluated by Cell Counting Kit-8 (CCK-8) cell proliferation assay, cell clone formation assay, and flow cytometry. Western blot, qRT-PCR, confocal microscope, RNA-sequencing, and transmission electron microscope were performed to assess lipid peroxidation and ferroptosis level of PDAC cells in the context of M1 macrophage or TNF-α.</p><p> Results: M1 macrophages inhibited cell proliferation and promoted cell death of PDAC cells, in which ferroptosis played a vital role. Mechanistically, Tumor Necrosis Factor-alpha (TNF-α) released by M1 macrophages binds to the TNFR1 receptor on pancreatic cancer cells, activating the p38 MAPK signaling, which upregulates Acyl-CoA Synthetase Long-chain family member 4 (ACSL4) expression, a critical lipid metabolism enzyme linked to ferroptosis, thereby promoting ferroptosis. Knockdown of ACSL4 or TNFR1 significantly reduced TNF-α-induced ferroptosis. Discussion: TNF-α is a major inflammatory cytokine and is mainly generated by macrophages and T lymphocytes. It is involved in many pathological processes, such as inflammatory diseases, autoimmune diseases, and cancer. Studies have shown that the administration of recombinant TNF-α can induce tumor regression in mice with sarcomas. In our study, systemic injection of TNF-α slowed the tumor growth in nude mice, but with no significant difference compared with the control group, which may partially be attributed to its angiogenic activity. TNF-α signals via two distinct membrane-binding receptors, TNFR1 and TNFR2, which regulate various diseases. In pancreatic cancer, the role of TNF-α is complex and poorly understood. In a previous study, Chopra et al. found that exogenous systemic administration of human TNF-α, which interacted with murine TNFR1, significantly increased overall tumor growth in the Panc02-PDAC model. Intriguingly, the loss of TNFR1 led to an impediment of immune cell infiltration into the tumor and impaired immunosurveillance, which accelerated tumor growth. This suggests that TNFR1 exerts both pro-tumoral and anti-tumoral functions in the Panc02-PDAC model, but the overall outcome is likely dependent on the spatiotemporal availability of TNF-α. However, systemic TNF-α injection can lead to severe side effects in animals, limiting its further application. In a recent study, TNFR2 was found to promote tumorigenesis and progression in the KPC-PDAC model. Knockdown of TNFR2 or pretreatment with an anti-TNFR2 antibody could significantly slow the tumor progression and incidence. In our study, TNFR2 was found to h","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Association Between Sleep Traits and Vertigo Risk: A Two-Sample Bidirectional Mendelian Randomization Study.","authors":"Weimin Xu, E Tian, Jun Wang, Xixi Yu, Zhaoqi Guo, Jingyu Chen, Sulin Zhang","doi":"10.2174/0115665240358943250612115854","DOIUrl":"https://doi.org/10.2174/0115665240358943250612115854","url":null,"abstract":"<p><p><p>Background: Observational studies suggest the potential association between sleep traits and vertigo; however, causal evidence remains limited. </p><p> Objective: This study aimed to explore the relationship between genetically predicted sleep traits and vertigo with the Mendelian randomization (MR) method.</p><p> Methods: Instrumental variables for sleep traits (snoring, sleep duration, insomnia, daytime sleepiness, daytime napping, and chronotype) were adopted from genomewide association studies (GWAS) data of European ancestry from UK Biobank. The summary-level datasets of vertigo were retrieved from the GWAS of FinnGen. Inversevariance weighted (IVW) method was adopted as the main analysis.</p><p> Results: IVW analysis revealed a significant association between genetically predicted daytime napping (OR = 1.51, 95% CI =1.08-2.12, P = 0.016) and chronotype (OR = 1.13, 95% CI =1.01-1.26, P = 0.033), both of which were associated with an increased risk of vertigo. However, we did not find evidence for a causal effect of snoring, overall sleep duration, long sleep duration, short sleep duration, insomnia, and excessive daytime sleepiness on vertigo. No reverse causality was detected.</p><p> Conclusion: Our findings suggest that abnormal sleep patterns may serve as risk factors for vertigo disorders and offer opportunities for the prevention and management of vertigo disorders.</p>.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma Sphingomyelin Levels Mediate the Causal Relationship Between Gut Microbiota and Myocardial Interstitial Fibrosis: A Mendelian Randomization Study.","authors":"Mingjun Yu, Xingxiao Huang, Beibei Gao, Jinyu Huang","doi":"10.2174/0115665240393776250523073829","DOIUrl":"https://doi.org/10.2174/0115665240393776250523073829","url":null,"abstract":"<p><p><p>Background: Prior studies established associations between gut microbiota and myocardial interstitial fibrosis. Nevertheless, the causal relationships and potential intermediaries remain unknown. Thus, we employed a Mendelian randomization strategy to explore whether gut microbiota causally influence myocardial interstitial fibrosis and to assess whether plasma metabolites serve as potential intermediaries in this pathway. </p><p> Methods: A two-sample Mendelian randomization approach was performed, utilizing genome-wide association studies to examine the causal relationship between gut microbiota (n= 18,340) and myocardial interstitial fibrosis (n=41,505). Additionally, an investigation was conducted to determine the potential mediation by four plasma metabolites (n=8,299) via a two-step Mendelian randomization analysis. Inverse variance weighted method was the primary method employed in Mendelian randomization, and complementary analyses were conducted alongside to enhance the robustness of the results.</p><p> Results: Mendelian randomization analysis indicated suggestive associations of three microbial taxa with myocardial interstitial fibrosis. The most significant taxon was the genus Faecalibacterium (β [SE], -0.1272 [0.0347], P = 0.0002). Reverse Mendelian randomization analyses revealed no evidence of myocardial interstitial fibrosis affecting these three microbial taxa. In the two-step Mendelian randomization analysis involving four plasma metabolites, it was found that plasma sphingomyelin levels mediated the causal effects of genus Faecalibacterium on myocardial interstitial fibrosis (proportion mediated = 14.2%, 95% CI = 1.4-27.0%).</p><p> Conclusion: The study validates the causality between particular gut microbial taxa and myocardial interstitial fibrosis, and suggests that plasma sphingomyelin might mediate this association. These findings offer a novel perspective on myocardial interstitial fibrosis prevention, and underscore the significance of plasma sphingomyelin in human health and disease.</p>.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of ARHGAP40 in Breast Cancer by Hypermethylation and its Clinical Significance.","authors":"Yumei Tao, Jingyu Wang, Xiaoyan Ren, Lili Gu, Jingjun Sun, Jiandong Wang","doi":"10.2174/0115665240370635250617210156","DOIUrl":"https://doi.org/10.2174/0115665240370635250617210156","url":null,"abstract":"<p><strong>Objective: </strong>ARHGAP40 is a Rho GTPase-activating protein (RhoGAP). The expression and biological roles of ARHGAP40 in breast cancer are unknown. We aimed to investigate the expression of ARHGAP40 and its epigenetic mechanism in breast cancer.</p><p><strong>Methods: </strong>The expression level of ARHGAP40 was examined in breast cancer cell lines and tissues. The methylation status of ARHGAP40 was analyzed using a bisulfite sequencing PCR (BSP). The biological roles of ARHGAP40 in breast cancer were investigated.</p><p><strong>Results: </strong>ARHGAP40 mRNA was significantly expressed in MCF-7 and weakly in MDA-MB-231, whereas methylated ARHGAP40 was detected in MDA-MB-231 and partly in MCF-7. ARHGAP40 protein was positively expressed in normal breast epithelial cells in all paracancerous tissues. The expression level of ARHGAP40 was significantly associated with age, TNM stage, lymph node metastasis, molecular subtypes, proliferative marker Ki67, and HER2 expression. The overall survival (OS) of patients with high expression of ARHGAP40 was longer than those with low expression. Overexpression of ARHGAP40 in MCF-7 and MDA-MB-231 cells induced apoptosis and suppressed cell proliferation. The opposite outcomes were observed in the ARHGAP40 knockdown experiment.</p><p><strong>Conclusion: </strong>Our data suggested ARHGAP40 to be downregulated in breast cancer due to hypermethylation. ARHGAP40 was found to act as a tumor suppressor in breast cancer and could be a potential therapeutic target for breast cancer.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression and Function of Vasopressin Receptors in the HT-29 Cell Line.","authors":"Beril Erdem Tuncdemır, Emel Saglar Ozer","doi":"10.2174/0115665240394070250703050642","DOIUrl":"https://doi.org/10.2174/0115665240394070250703050642","url":null,"abstract":"<p><strong>Introduction: </strong>Vasopressin receptors can have different effects on tumorigenesis. The in vitro usage of agonists and antagonists of these receptors can also have a potential impact on developing adjuvant treatment options. Therefore, we aimed to demonstrate the expression and function of vasopressin receptors in the HT- 29 cell line, which is one of the cell lines frequently used in colorectal cancer studies. Colorectal cancer is one of the most prevalent cancer types worldwide. There are many risk factors for colorectal cancer, including unhealthy lifestyle and social environment, and early diagnosis can enhance the survival of patients. Main treatment strategies aim to slow down the progression of cancer, increase survival, and enhance the quality of life. Investigating the relationship between colorectal cancer and vasopressin receptors has been an interesting research area in terms of developing new treatment strategies lately.</p><p><strong>Methods: </strong>For receptor expression and functional analysis, RT-PCR experiments and cAMP accumulation assay were performed.</p><p><strong>Results: </strong>The expression of V2R and V1aR was observed in HT-29 cells, and V2Rs demonstrated their function as cAMP responders after treatment with agonists and antagonists.</p><p><strong>Discussion: </strong>This is the first study to report that V2R and V1aR expressions were detected by RT-PCR, and the functionality of V2R was analyzed by cAMP accumulation assay after treating HT-29 cells with agonists and antagonists.</p><p><strong>Conclusion: </strong>We hope that these results may contribute to colorectal cancer research and the development of novel therapeutic strategies targeting vasopressin receptor signaling pathways.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comparative Review of Methods for Detecting Epidermal Growth Factor Receptor Mutations in Cell-Free DNA from Lung Cancer Patients.","authors":"Sepideh Shohani, Mahmood Barati, Arshad Hosseini","doi":"10.2174/0115665240374769250703232841","DOIUrl":"https://doi.org/10.2174/0115665240374769250703232841","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer remains the leading cause of cancer-related mortality. Determining the T790M resistance variants and epidermal growth factor receptor (EGFR) mutations is crucial for personalized treatment, especially when using targeted therapies.</p><p><strong>Objective: </strong>This review article aims to comprehensively compare some of the various diagnostic techniques associated with liquid biopsies, such as cell-free DNA (cfDNA) for T790M and EGFR mutant identification. It also aims to evaluate their pertinence in clinical settings, as well as their sensitivity and specificity to determine how effectively they monitor treatment response and resistance.</p><p><strong>Methods: </strong>A literature search was conducted using databases including PubMed, Scopus, and Web of Science. The keyword list included \"EGFR mutations,\" \"T790M resistance,\" \"liquid biopsy,\" \"COLD PCR,\" \"NGS,\" \"ddPCR,\" \"BEAMing,\" and other methods. The effect of these studies on diagnostic technologies for identifying EGFR mutations was assessed in terms of clinical practice, methodological accuracy, and significance. Sensitivity, specificity, clinical applicability, cost analysis, turnaround times, and ease of integration into clinical workflows were used as parameters for evaluation based on the literature.</p><p><strong>Results: </strong>There are advantages and disadvantages to cfDNA monitoring strategies for treatment response and resistance, as well as to the assessment of sensitivity, specificity, and clinical applicability for identifying EGFR mutations.</p><p><strong>Conclusion: </strong>Advanced techniques such as COLD-PCR, LC-MS, qPCR, NGS sequencing, Sanger sequencing, PNA microarrays, the Allele-Specific Competitive Extension (ASCE) real-time PCR assay, and nanopore technology are necessary for personalized lung cancer management. However, depending on the objective of the work, the suitable method should be selected based on its benefits and drawbacks.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanosensitive Ion Channel Piezo1 Promotes Obliterative Bronchiolitis through YAP-Dependent Epithelial-to-Mesenchymal Transition.","authors":"Li Wan, You Wu, Jingsong Yang, Peng Deng, Zuhuan Yao, Quanchao Sun","doi":"10.2174/0115665240377965250701114255","DOIUrl":"https://doi.org/10.2174/0115665240377965250701114255","url":null,"abstract":"<p><strong>Introduction: </strong>Obliterative bronchiolitis (OB) is a severe and progressive complication characterized by the fibrotic obliteration of small airways, leading to significant morbidity and mortality, particularly in lung transplant recipients. The pathogenesis of OB involves complex cellular processes, among which epithelial-tomesenchymal transition (EMT) plays a crucial role. This study investigates the role of mechanosensitive ion channel Piezo1 in promoting OB through Yes-associated protein (YAP)-dependent EMT.</p><p><strong>Method: </strong>Piezo1-induced signal pathway alterations, fibrosis, and EMT-related features were examined in the mouse OB model and BEAS-2B cells. The efficacy of Piezo1 in EMT and OB was explored and validated both in vitro and in vivo.</p><p><strong>Results: </strong>Piezo1 was found to be upregulated in OB, and pharmacological inhibition of Piezo1 effectively alleviated EMT and fibrotic deposition. Piezo1 activation stimulated the Ca2+ influx and nuclear translocation of YAP that triggered the transition of epithelial cells into a mesenchymal phenotype, which contributed to airway fibrosis and obstruction. Furthermore, inhibition of YAP or calcium chelation significantly attenuated Piezo1 activation-induced EMT and OB, indicating that YAP and Ca2+ are critical mediators in this process.</p><p><strong>Discussion: </strong>Piezo1 expression was found to be upregulated in OB, and its activation induced the epithelial-to-mesenchymal transition (EMT) process via a YAP-dependent pathway. Piezo1 could accelerate EMT and the occlusion rate of grafts via Ca2+ influx-dependent YAP activation in OB, suggesting a direct role in facilitating EMT and subsequent fibrotic remodeling in OB.</p><p><strong>Conclusion: </strong>The present results highlight that Piezo1 promotes OB through a YAPdependent EMT pathway, suggesting Piezo1 as a novel therapeutic strategy for treating OB and potentially improving outcomes of lung transplant recipients.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLC41A2 Suppresses Colon Cancer Progression by Inhibiting GSK3β Ubiquitin-proteasome Degradation.","authors":"Yueyao Lu, Ying Shen, Jinsong Liu, Jianzhong Deng, Yue Wang, Qian Liu, Wenbin Lu","doi":"10.2174/0115665240397574250630060947","DOIUrl":"https://doi.org/10.2174/0115665240397574250630060947","url":null,"abstract":"<p><strong>Background: </strong>Colon cancer is a highly prevalent tumor with a high mortality rate worldwide. SLC41A2 is a member of the solute carrier family, but its role in colon cancer is still unclear.</p><p><strong>Methods: </strong>The relationship between the expression level of SLC41A2 and clinicopathological features in colon cancer was investigated using data from the TCGA database. The differential expression genes of SLC41A2 were identified the potential role of SLC41A2 in colon cancer was analysed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. By transfecting plasmids or siRNA to overexpress or knock down SLC41A2 in colon cancer cells, the effects of SLC41A2 on colon cancer cell proliferation, migration, and apoptosis were detected through EdU, MTT, wound-healing, Transwell, and JC-1 experiments. Western blot and ubiquitination experiments validated the regulation of GSK3β stability by SLC41A2. Rescue experiments and CCK8 assays confirmed the regulatory effect of SLC41A2 on GSK3β.</p><p><strong>Results: </strong>Compared to normal tissues, SLC41A2 exhibited a lower expression level in colon cancer, and the expression levels of SLC41A2 were correlated with the stage and Tumor Node Metastasis (TNM) classification. GO and KEGG analyses displayed that SLC41A2 primarily affected the growth factor activity and Wnt signaling pathway. Furthermore, elevated expression of SLC41A2 notably decreased the proliferation, migration and invasion of colon cancer cells, along with increased apoptosis. The overexpression of SLC41A2 and rescue experiments confirmed that SLC41A2 enhances the protein stability of GSK3β by inhibiting its ubiquitin-proteasome degradation and causes the upregulation of GSK3β, thereby suppressing the progression of colon cancer.</p><p><strong>Conclusion: </strong>SLC41A2 was lowly expressed in colon cancer tissues or cells. By inhibiting the ubiquitin-proteasome degradation of GSK3β, SLC41A2 can significantly upregulate the expression of GSK3β, which ultimately suppresses the proliferation and migration of colon cancer cells.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triple Negative Breast Cancer Heterogeneity and Tumour Microenvironment- based Model Systems' Focus on Druggable Targets.","authors":"Shreyasi Kundu, Suresh P K","doi":"10.2174/0115665240387430250508080548","DOIUrl":"https://doi.org/10.2174/0115665240387430250508080548","url":null,"abstract":"<p><p>Fifteen to twenty percent of all cases of breast cancer are TNBC (triple negative breast cancer) and exhibit heterogenic features due to their diverse molecular characteristics. Additionally, their aberrant cell cycling behavior contributes to their metastatic capabilities and aggressive nature. TNBC is the only molecular subtype, which lacks the expression of hormone receptors, like estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2). Hence, it is recalcitrant to hormone therapy. Also, the complex and evolving tumour microenvironment (TME) comprises blood vessels, stromal cells, immune cells, metabolic factors, extracellular matrix (ECM), and an integrated perspective of their interconnections as well as their variability with respect to TNBC progression needs to be comprehended for biomarker/druggable target(s) development and/or their validation. Such TME-based model systems can help us understand the relationship between the different TME components that affect tumour growth and metastasis. This review also catalogs biomarkers and TNBC behaviour within the TME. Also, this review discusses and analyses models that replicate various tumour subtypes that can be correlated with variability in treatment responses, thereby facilitating a better understanding of TNBC heterogeneity. Thus, by identifying biomarkers and constructing model systems, we can augment efforts to overcome treatment failure and poor outcomes in TNBC patients. These subtype-specific TNBC model systems, mirroring the intricacies of the TME, have the potential to provide a feasible and innovative approach to target TNBC cells. This review will facilitate the ongoing global efforts to develop efficacious and safe \"tailor-made\" drugs for TNBC patients.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut Microbiota-Induced Long Non-Coding RNA Snhg9 Regulates the Development of Human Malignant Tumors.","authors":"Dengke Jia, Yaping He, Qianle Chen, Yawu Zhang","doi":"10.2174/0115665240366916250629064055","DOIUrl":"https://doi.org/10.2174/0115665240366916250629064055","url":null,"abstract":"<p><p>Gut microbes influence the progression of human malignancies through their recognition by the immune system and their effects on numerous metabolic pathways. Long non-coding RNA is a key target of intestinal microbiota involved in the progression of human malignant tumors. Current research shows that there is a close cross-talk between long non-coding RNA Snhg9 and intestinal microorganisms, and it is widely involved in the progression of human malignant tumors. An in-depth study of the interaction between long non-coding RNA and intestinal flora and the intrinsic regulatory mechanism of snhg9 will provide new and powerful therapeutic targets for future research on human malignant tumors.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}