Molecular medicine reports最新文献

{"title":"Epigenetic downregulation of the proapoptotic gene <i>HOXA5</i> in oral squamous cell carcinoma.","authors":"Ying-Ju Chen, Shin-Wei Liao, Yen-Ling Lai, Yu-Fen Li, Yin-Che Lu, Chien-Kuo Tai","doi":"10.3892/mmr.2024.13421","DOIUrl":"https://doi.org/10.3892/mmr.2024.13421","url":null,"abstract":"<p><p>Homeobox A5 (<i>HOXA5</i>) has been identified as a tumor suppressor gene in breast cancers, but its role in oral squamous cell carcinoma (OSCC) has not been confirmed. The Illumina GoldenGate Assay for methylation identified that DNA methylation patterns differ between tumorous and normal tissues in the oral cavity and that <i>HOXA5</i> is one of the genes that are hypermethylated in oral tumor tissues. The present study obtained more‑complete information on the methylation status of <i>HOXA5</i> by using the Illumina Infinium MethylationEPIC BeadChip and bisulfite sequencing assays. The results indicated that <i>HOXA5</i> hypermethylation has great potential as a biomarker for detecting OSCC. Comparing <i>HOXA5</i> RNA expression between normal oral tissue and OSCC tissue samples indicated that its median level was 2.06‑fold higher in normal tissues that in OSCC tissues. Moreover, treatment using the demethylating agent 5‑aza‑2'‑deoxycytidine can upregulate <i>HOXA5</i> expression in OSCC cell lines, verifying that the silencing of <i>HOXA5</i> is primarily regulated by its hypermethylation. It was also found that upregulation of <i>HOXA5</i> expression can not only increase OSCC cell death but that it can also enhance the therapeutic effect of cisplatin both <i>in vitro</i> and <i>in vivo</i>, suggesting that <i>HOXA5</i> is an epigenetically downregulated proapoptotic gene in OSCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Limb remote ischemic post‑conditioning reduces injury and improves long‑term behavioral recovery in rats following subarachnoid hemorrhage: Possible involvement of the autophagic process.","authors":"Xiang Hu, Tao Lv, Shao-Feng Yang, Xiao-Hua Zhang, Yi-Feng Miao","doi":"10.3892/mmr.2024.13419","DOIUrl":"https://doi.org/10.3892/mmr.2024.13419","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the attention of the Editorial Office that the 'Sham' brain image featured in Fig. 1B on p. 23 was strikingly similar to an image that was published subsequently in the journal <i>Scientific Reports</i>, whereas the control TUNEL assay data shown in Fig. 4A on p. 25 were similarly strikingly similar to data shown in a paper published previously in the journal <i>Mediators of Inflammation</i>, even though the overall experiments portrayed in the other journals were different. As the three affected articles did hold at least one author in common, we asked the authors to provide an explanation to account for the sharing of these data among these papers, but no reply was forthcoming from them; therefore, in the absence of a reply from these authors, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 21‑30, 2018; DOI: 10.3892/mmr.2017.7858].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEDD4 enhances bone‑tendon healing in rotator cuff tears by reducing fatty infiltration.","authors":"Jian Li, Ying Peng, Dong Zhen, Caifen Guo, Wuxun Peng","doi":"10.3892/mmr.2024.13420","DOIUrl":"https://doi.org/10.3892/mmr.2024.13420","url":null,"abstract":"<p><p>Rotator cuff tears (RCT) can cause shoulder pain, weakness and stiffness, significantly affecting daily life. Analysis of the GSE103266 dataset revealed significant changes in the mTOR/PI3K/Akt signaling pathway and lipid metabolism‑related pathways, suggesting that fatty infiltration may affect RCT. The analysis indicated that the ubiquitin ligase NEDD4 plays a critical role in RCT. NEDD4 was found to be highly associated with the mTOR/PI3K/Akt signaling pathway. An RCT model in Sprague‑Dawley (SD) rats was established to study the role of NEDD4 in regulating the mTOR pathway and investigate its effects on fatty infiltration. SD rats were divided into NEDD4 overexpression and knockout groups. Tissue recovery, apoptosis and fat deposition were measured through histological staining, reverse transcription‑quantitative PCR and western blotting. Additionally, cell culture of fibro‑adipogenic progenitors and lentiviral transfection were conducted to investigate the effect of NEDD4 on adipocyte differentiation. NEDD4 overexpression significantly reduced lipid accumulation, whereas NEDD4 knockdown enhanced lipid accumulation. NEDD4 was found to regulate the mTOR pathway and the expression of adipogenesis‑related genes, promoting fat metabolism and inhibiting adipocyte differentiation. Histological analysis indicated that NEDD4 overexpression improved tissue recovery and reduced apoptosis. Targeting NEDD4 offers a potential therapeutic strategy to improve the clinical outcomes of patients with RCT by modulating the mTOR pathway and fat metabolism.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue factor signalling modifies the expression and regulation of G1/S checkpoint regulators: Implications during injury and prolonged inflammation.","authors":"Sophie J Featherby, Eamon C Faulkner, Camille Ettelaie","doi":"10.3892/mmr.2024.13404","DOIUrl":"10.3892/mmr.2024.13404","url":null,"abstract":"<p><p>Tissue factor (TF) possesses additional physiological functions beyond initiating the coagulation cascade. Cellular signals initiated by cellular TF or on contact with TF‑containing microvesicles, contribute to wound healing through regulating a number of cellular properties and functions. TF regulates the cell cycle checkpoints, however the underlying signalling mechanisms have not been determined. Endothelial (human dermal blood endothelial cells and human umbilical vein endothelial cells) and epithelial [human telomerase reverse transcriptase‑human pancreatic nestin‑expressing ductal cells (hTERT‑HPNE) and AsPC‑1] cells were exposed to different concentrations of recombinant TF, and the influence on G1/S checkpoint regulators examined. Short‑term exposure to a lower concentration of TF promoted increased p16^INKa and decreased p21^CIP1/WAF1 expression, together with higher early region 2 binding factor (E2F) transcriptional activity and increased phosphorylation of Thr821/826 within retinoblastoma protein, leading to cell proliferation. The increase in p16^INKa expression was prevented following inhibition of β1‑integrin, or blocking the exosite within TF with AIIB2 and 10H10 antibodies, respectively. Exposure of cells to higher concentrations of TF induced disproportionate increases in p16^INKa and p21^CIP1/WAF1 expression, reduced retinoblastoma protein phosphorylation and E2F activity. Prolonged treatment of the immortalised hTERT‑HPNE cells with recombinant TF, resulted in significant downregulation of p16^INKa protein, which was partially due to reduced mRNA expression, together with increased E2F activity, and cyclin E mRNA expression. Although an increase in the methylation of the p16^INKa promoter was detected, the reduction in p16^INKa protein was concurrent with, and partly attributed to increased p14^ARF expression. TF appears early at the site of trauma, and its concentration is an ideal gauge for determining the extent of cellular damage, initiating clearance and repair. It is hypothesised that the balance of this signal is also dependent on the ability of cells to moderate the TF, and therefore on the level of damage. However, prolonged exposure of cells for example due to inflammation, leads to the dysregulation of the G1/S checkpoint by the tumour suppressors, leading to aberrant growth.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Tanshinone II A stabilizes vulnerable plaques by suppressing RAGE signaling and NF‑κB activation in apolipoprotein‑E‑deficient mice.","authors":"Dong Zhao, Lufang Tong, Lixin Zhang, Hong Li, Yingxin Wan, Tiezhong Zhang","doi":"10.3892/mmr.2024.13410","DOIUrl":"10.3892/mmr.2024.13410","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blotting data shown in Fig. 4B on p. 4988 had already appeared in an article written by different authors at different research institutes that had already been published. In addition, it appeared as if some of the control β‑actin protein bands had been re‑used in Fig. 3 on p. 4987, comparing between Fig. 3A and C.  Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 14: 4983‑4990, 2016; DOI: 10.3892/mmr.2016.5916].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1 regulates cigarette smoke extract‑induced alveolar macrophage polarization and inflammation by inhibiting the TRAF6/NLRP3 signaling pathway.","authors":"Fang Yang, Huiping Qin, Chaoqun Qin, Bing Huang, Feng Gao, Yi Liao, Yanping Tang, Yanju Mo, Qianjie Yang, Changming Wang","doi":"10.3892/mmr.2024.13408","DOIUrl":"10.3892/mmr.2024.13408","url":null,"abstract":"<p><p>M1 macrophages activated by cigarette smoke extract (CSE) serve a pro‑inflammatory role in chronic obstructive pulmonary disease (COPD). The expression of silent information regulator 1 (SIRT1) is decreased in the alveolar macrophages of patients with COPD. However, whether SIRT1 is involved in COPD by regulating macrophage polarization remains unknown. Rat Alveolar Macrophage NR8383 cells were exposed to CSE. Cell Counting Kit‑8 assay, western blot assay and ELISA showed that with increasing concentration of CSE, the activity of NR8383 cells and expression of SIRT1 gradually decreased, while the release of inflammatory cytokines TNFα, IL‑1β and IL‑6 increased. As shown in western blot or Immunofluorescence assays, exposure to CSE also increased expression levels of the M1 markers inducible nitric oxide synthase and CD86, whereas it downregulated expression of the M2 markers arginase 1 and CD206. In addition, CSE increased expression of TNF receptor associated factor 6 (TRAF6), NOD‑like receptor thermal protein domain associated protein 3 (NLRP3) and cleaved caspase‑1 protein in NR8383 cells. Overexpression plasmids of SIRT1 and TRAF6 significantly reversed the aforementioned changes induced by CSE. Moreover, immunoprecipitation demonstrated that TRAF6 could bind to NLRP3. The overexpression of TRAF6 notably attenuated the regulatory effects of overexpression of SIRT1 on polarization and inflammation in NR8383 cells. Conversely, overexpression of SIRT1 inhibited the TRAF6/NLRP3 signaling pathway, thereby suppressing CSE‑induced M1 polarization and release of inflammatory factors in NR8383 cells. The present study demonstrates that SIRT1 regulates CSE‑induced alveolar macrophage polarization and inflammation by inhibiting the TRAF6/NLRP3 signaling pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The combination of serum lncRNA PTTG3P and mRNA PTTG1 serves as a diagnostic and prognostic marker for hepatocellular carcinoma.","authors":"Shunwang Cao, Fei Zhong, Xueying Chen, Sikai Ke, Xiangrong Zhong, Tingting Li, Yanhua Sha, Chunmin Kang, Sheng Qin, Hongmei Wang, Yi Wang, Shuzhi Liao, Peifeng Ke","doi":"10.3892/mmr.2024.13409","DOIUrl":"10.3892/mmr.2024.13409","url":null,"abstract":"<p><p>Long noncoding RNA (lncRNA) PTTG3P has been demonstrated to participate in the development of hepatocellular carcinoma (HCC) by targeting the mRNA PTTG1. The present study aimed to investigate the diagnostic efficacy of serum lncRNA PTTG3P, mRNA PTTG1 and their combination for the diagnosis and prognosis of HCC. A total of 373 participants were enrolled in the present study, including 73 patients with HCC, 100 patients with chronic hepatitis B (CHB), 100 patients with liver cirrhosis (LC) and 100 healthy controls (HCs). The expression levels of serum RNAs were quantified by reverse transcription‑quantitative PCR. The association between serum lncRNA PTTG3P and clinical characteristics was further analyzed. Receiver operating characteristic (ROC) curve and area under curve (AUC) analyses were performed to estimate the diagnostic ability of serum lncRNA PTTG3P, PTTG1 and their combinations with other biomarkers for HCC. The results revealed that the expression levels of lncRNA PTTG3P and mRNA PTTG1 were markedly increased in the serum of patients with HCC and CHB compared with in the serum of HCs. Additionally, the postoperative levels of lncRNA PTTG3P and mRNA PTTG1 were significantly lower than the preoperative concentrations in 36 paired patients with HCC. Spearman's correlation coefficient analysis showed that serum lncRNA PTTG3P was correlated with aspartate transaminase (AST). ROC analysis showed that both lncRNA PTTG3P and mRNA PTTG1 had a significant predictive value for HCC. The AUC values of lncRNA PTTG3P and mRNA PTTG1 alone were 0.636 and 0.634, respectively. Furthermore, combining lncRNA PTTG3P, mRNA PTTG1, α‑fetoprotein (AFP), alanine aminotransferase (ALT), AST, γ‑glutamyl transpeptidase (GGT) and alkaline phosphatase (ALP) significantly increased the AUC value. The best performance was the combination of PTTG3P, PTTG1, AFP, ALT, AST, GGT and ALP with an AUC of 0.959, a sensitivity of 90.4% and a specificity of 98.0%. In conclusion, the combination of serum lncRNA PTTG3P, mRNA PTTG1 and AFP appeared to be a noninvasive biomarker with comparatively high specificity and sensitivity for the diagnosis of HCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF‑1α overexpression improves the efficacy of human induced pluripotent stem cell‑derived cardiomyocytes for cardiac repair following myocardial infarction.","authors":"Jianfeng Du, Tianbao Wang, Liqing Xu","doi":"10.3892/mmr.2024.13405","DOIUrl":"10.3892/mmr.2024.13405","url":null,"abstract":"<p><p>Myocardial infarction (MI) is the leading cause of death worldwide and currently there are limited therapies that can regenerate the lost cardiac cells following MI. To enhance the therapeutic effects of human induced pluripotent stem cell‑derived cardiomyocytes (hiPSC‑CM) transplantation for treatment of MI, the present study sought to increase the pro‑angiogenic effect of hiPSC‑CM by overexpressing a mutated hypoxia‑inducible factor 1‑alpha (HIF‑1α; P402A; P564A) via lentivirus transfection. Morphology and the electrophysiology of the genetically engineered cell were both unchanged. The present study demonstrated that the proangiogenic factors in the conditioned medium of the HIF‑1α‑overexpressing hiPSC‑CM (HIF‑CM) were upregulated and subsequently resulted to the rescue of the tube forming ability and migratory ability of the hypoxia‑injured human umbilical vein endothelial cells. Using a MI mouse model, the present study demonstrated that the transplantation of HIF‑CM greatly improved cardiac function, decreased scar size, promoted the concentration of the proangiogenic factors in circulation and promoted the neovessel formation in mice with MI. In conclusion, HIF‑1α‑overexpressing hiPSC‑CM could increase the angiogenesis of endothelial cells and mediate cardioprotection in mouse following MI.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis in schizophrenia: Mechanisms and therapeutic potentials (Review).","authors":"Shuang Lv, Chunxia Luo","doi":"10.3892/mmr.2024.13402","DOIUrl":"10.3892/mmr.2024.13402","url":null,"abstract":"<p><p>Schizophrenia, a complex psychiatric disorder, presents with multifaceted symptoms and important challenges in treatment, primarily due to its pathophysiological complexity, which involves oxidative stress and aberrant iron metabolism. Recent insights into ferroptosis, a unique form of iron‑dependent cell death characterized by lipid peroxidation and antioxidant system failures, open new avenues for understanding the neurobiological foundation of schizophrenia. The present review explores the interplay between ferroptosis and schizophrenia, emphasizing the potential contributions of disrupted iron homeostasis and oxidative mechanisms to the pathology and progression of this disease. The emerging evidence linking ferroptosis with the oxidative stress observed in schizophrenia provides a compelling narrative for re‑evaluating current therapeutic strategies and exploring novel interventions targeting these molecular pathways, such as the glutathione peroxidase 4 pathway and the ferroptosis suppressor protein 1 pathway. By integrating recent advances in ferroptosis research, the current review highlights innovative therapeutic potentials, including N‑acetylcysteine, selenium, omega‑3 fatty acids and iron chelation therapy, which could address the limitations of existing treatments and improve clinical outcomes for individuals with schizophrenia.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Solamargine inhibits gastric cancer progression via inactivation of STAT3/PD‑L1 signaling.","authors":"Xiongxiang Liu, Lin Song, Wen Liu, Bin Liu, Lang Liu, Yao Su","doi":"10.3892/mmr.2024.13400","DOIUrl":"10.3892/mmr.2024.13400","url":null,"abstract":"<p><p>Gastric cancer (GC) is characterized by a high mortality rate (70%) worldwide. Programmed cell death‑1 and its ligand, programmed cell death ligand 1 (PD‑L1), are vital immune checkpoints, which serve a notable role in GC. Solamargine, an extract from traditional Chinese medicine Long Kui, exerts suppressive effects on several types of cancer including cervical, lung and prostate cancer. However, the association between solamargine and PD‑L1 in GC remains unclear. Therefore, the present study aimed to investigate the underlying mechanism of solamargine on GC. Specifically, 5‑ethynyl‑2'‑deoxyuridine and Transwell assays were performed to assess GC cell proliferation, invasion and migration. Additionally, GC cells (HGC‑827 and NCI‑N87) were stimulated with 20 ng/ml recombinant human IL‑6 for 24 h, before the protein expression levels of PD‑L1 were measured using western blot analysis. Furthermore, T cell function was evaluated through incubation of Jurkat T cells with solamargine. The results demonstrated that solamargine could markedly inhibit GC cell proliferation, migration and invasion, by inhibiting STAT3 signaling. In addition, GC cell treatment with solamargine downregulated the expression of PD‑L1. Furthermore, solamargine reversed the IL‑6‑induced PD‑L1 upregulation in GC cells by downregulating STAT3 activity. Additionally, the results demonstrated that solamargine inhibited IL‑6‑induced PD‑L1 upregulation of GC cells. This suggests that solamargine exerted an immunostimulatory activity in GC. In conclusion, the present study indicated that solamargine may inhibit the progression of GC by suppressing STAT3/PD‑L1 signaling. Therefore, treatment with solamargine may serve as novel strategy for the treatment of GC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}