Cancer Cell International最新文献

{"title":"Genetically engineered bacteria-based nanocomposite synergistic HIFU for tumor therapy by changing the acoustic environment of tumor tissues.","authors":"Ting Gong, Wen Zhao, Youqiang Chen, Youqian He, Jie Xiong, Yijun Xiong, Liu Yin, Yong Luo, Yi Tang","doi":"10.1186/s12935-025-03833-8","DOIUrl":"10.1186/s12935-025-03833-8","url":null,"abstract":"<p><p>High-intensity focused ultrasound (HIFU) is a novel non-invasive technique with tremendous potential applications. However, ensuring effectiveness and safety of HIFU therapy remains a substantial challenge. Changing the acoustic environment of tumor tissues is an emerging way to solve this problem. In this study, we successfully constructed a bacteria-based nanocomposite, consisting genetically engineered bacteria (GVs-E.coli) and perfluorohexane/poly(lactic-co-glycolic acid) (PFH/PLGA) nanoparticles, which is denoted as GVs-E@PP NPs. We demonstrated that GVs-E@PP NPs could selectively target and proliferate in the tumor sites, and enhance the efficacy of HIFU therapy by changing the acoustic environment of tumor tissues. Specifically, they induced an increase in collagen fibers, elastic modulus, sound velocity and sound attenuation within tumor tissues, while simultaneously reducing tumor angiogenesis. These comprehensive changes facilitated the therapeutic efficacy of HIFU treatment. In summary, this approach represents an innovative therapeutic strategy to enhance HIFU synergy in tumor treatment.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"201"},"PeriodicalIF":5.3,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12135489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pericytes in castration-resistant prostate cancer associated with disease progression and immunotherapy response: insights from single-cell analysis.","authors":"Yifeng Qiu, Yuhan Wang, Jiahe Liu, Kai Sun, Shigeo Horie, Zhitong Bing, Qi Hou","doi":"10.1186/s12935-025-03838-3","DOIUrl":"10.1186/s12935-025-03838-3","url":null,"abstract":"<p><strong>Background: </strong>The current immunotherapeutic strategies yield limited therapeutic benefits in patients with castration-resistant prostate cancer (CRPC) due to its immunologically \"cold\" tumor milieu. Pericytes play a pivotal role in facilitating metastatic dissemination and modulating immune response in malignancies. Our investigation is designed to decipher the biological effects of pericytes on CRPC and their interactions with the tumor microenvironment.</p><p><strong>Methods: </strong>We leveraged single-cell transcriptomics and immunofluorescence staining to ascertain the presence and spatial distribution of pericytes in prostate cancer (PCa). Subsequently, we thoroughly delineated the phenotypic and functional characteristics of the CRPC-pericytes subpopulation. The clinical and prognostic significance of CRPC-pericytes was assessed by employing several bulk RNA-seq and microarray datasets. Additionally, we examined the association between the abundance of CRPC-pericytes and immunological features in the PCa microenvironment. Furthermore, the RM-1 subcutaneous tumor model was leveraged to assess the synergistic efficacy of platelet-derived growth factor (PDGF) signaling inhibition in conjunction with immunotherapeutic interventions.</p><p><strong>Results: </strong>We discerned pericytes according to their marker genes and observed the α-SMA-positive pericytes encircling the vasculature in PCa and adjacent normal tissues. In the CRPC-pericytes subpopulation, a pronounced upregulation of PDGF signaling and angiogenesis was observed, whereas antitumor immunity-related pathways were suppressed. In addition, CRPC-pericytes displayed notably enhanced interactions with endothelial cells, fibroblasts, and myeloid cells, compared to PCa-pericytes. Patients with elevated prevalence of CRPC-pericytes exhibited notably reduced recurrence-free survival and unresponsiveness to immunotherapeutic interventions. Moreover, CRPC-pericytes were positively associated with immunosuppressive properties of the TME. Notably, combinatorial application of PDGFR inhibitor and anti-PD-1 therapy elicited substantial synergistic antitumor effects in murine PCa models.</p><p><strong>Conclusion: </strong>Our investigation uncovers a CRPC-pericytes subpopulation implicated in cancer progression and immunosuppression, suggesting that therapies targeting the phenotypic transition of pericytes could act synergistically with immunotherapeutic regimens to improve survival rates in CRPC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"200"},"PeriodicalIF":5.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12135593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidptosis in pediatric AML: a multi-omics approach to risk stratification and potential therapeutic strategy.","authors":"Yichen Lei, Jiasi Zhang, Yaqin Wang, Aiguo Liu","doi":"10.1186/s12935-025-03824-9","DOIUrl":"10.1186/s12935-025-03824-9","url":null,"abstract":"<p><strong>Background: </strong>The evolving molecular portrait of acute myeloid leukemia (AML) has exposed previously unrecognized cell death programs that fuel disease progression and treatment resistance-uncovering untapped therapeutic potential. Recent work has uncovered disulfidptosis-a novel form of programmed cell death (PDC) triggered by glucose deprivation in SLC7A11-high AML cells-as a potential therapeutic vulnerability. However, disulfidptosis in pediatric AML (pAML) remains largely unexplored, with no comprehensive studies assessing its biological significance or clinical prognostic value.</p><p><strong>Method: </strong>Here, we systematically characterize disulfidptosis in pediatric AML through multi-omics integration. Using ssGSEA, we quantified PDC patterns across bulk and single-cell transcriptomes, revealing distinct molecular subtypes via unsupervised clustering. Machine learning deciphered the biological networks underlying disulfidptosis, while in vitro experiments were performed to further validate.</p><p><strong>Results: </strong>In this study, we demonstrated that elevated disulfidptosis scores were associated with poor prognosis and a hypermetabolic state. Notably, patients carrying different driver mutations exhibited distinct levels of disulfidptosis susceptibility. Through in vitro experiments utilizing both cell lines and primary patient-derived cells, we found that elevated expression of SLC7A11, a key regulator of disulfidptosis, correlated with chemoresistance. Furthermore, disulfidptosis signatures effectively stratified risk subgroups in pAML, revealing a novel subtype, DSP3, characterized by prominent disulfidptosis features, an immune-desert tumor microenvironment, and an unfavorable prognosis. Additionally, our in vitro experiments identified the GLUT1 inhibitor STF-31 and the mitochondrial-targeted agent darinaparsin as potential therapeutic options for DSP3 patients, and combining with conventional chemotherapy exhibited a synergistic anti-tumor effect.</p><p><strong>Conclusion: </strong>In summary, this study employed multi-omics analysis to examine the characteristics of pAML in the context of disulfidptosis, identifying a novel disulfidptosis-related subtype, aiming to provide new insights for future studies on optimizing traditional regimen based on pAML pathogenesis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"199"},"PeriodicalIF":5.3,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12131395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NSC632839 suppresses esophageal squamous cell carcinoma cell proliferation in vitro by triggering spindle assembly checkpoint-mediated mitotic arrest and CREB-Noxa-dependent apoptosis.","authors":"Shan Zhao, Guihong Dong, Yixuan Guo, Yaxin Sun, Miaomiao Li, Beibei Sha, Wenjing Huang, Yuan Zhang, Yue Du, Jie Yan, Yangcheng Ma, Ruiyi Yang, Jianxiang Shi, Pei Li, Tao Hu, Ping Chen","doi":"10.1186/s12935-025-03831-w","DOIUrl":"10.1186/s12935-025-03831-w","url":null,"abstract":"<p><strong>Objective: </strong>Esophageal cancer is one of the most common digestive cancers in the world. Because of the limitation and resistence of the traditional chemotherapy drugs, it is important to explore new therapeutic targets and strategies for this refractory cancer. Recently, targeting deubiquitinases has emerged as a promising avenue for the development of anti-tumor drugs. However, the role and underlying mechanism of NSC632839, a broad-spectrum deubiquitinases inhibitor, in esophageal squamous cell carcinoma in vitro remain elusive.</p><p><strong>Methods: </strong>Cell Counting Kit-8 assay, colony formation assay, EdU proliferation experiment and cell morphology observation were used to detect the effect of NSC632839 on cell growth. Flow cytometry was employed to detect cell apoptosis and cell cycle arrest. Immunoblot and immunofluorescence was used to evaluate the expression level of cell cycle-, apoptosis-, and autophagy-related proteins.</p><p><strong>Results: </strong>NSC632839 inhibited the proliferation of Kyse30 and Kyse450 cells. Mechanistically, NSC632839 induced the formation of multipolar spindles, and its concomitant spindle assembly checkpoint-dependent mitotic arrest, followed by CREB-Noxa-mediated apoptosis. Reversine, a classical MPS1 kinase inhibitor known for its ability to inhibit the spindle assembly checkpoint, could rescue NSC632839-induced cell cycle arrest and apoptosis. Additionally, NSC632839 could trigger pro-survival autophagy. Combination of autophagy inhibitor, CQ and BafA1, with NSC632839 could induce stronger cell proliferation inhibition and apoptosis than NSC632839 alone.</p><p><strong>Conclusions: </strong>These findings provided a novel anti-cancer mechanism of NSC632839 and highlighted it as a potential anti-tumor agent for the treatment of esophageal cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"198"},"PeriodicalIF":5.3,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Venetoclax synergizes with Wnt/β-catenin inhibitor C-82 in acute myeloid leukemia by increasing the degradation of Mcl-1 protein.","authors":"Mengya Pan, Changqing Jiao, Menghua Sun, Duo Jin, Yin Wang, Haoxuan Wu, Yan Zhang, Enbo Chen, Bobin Su, Junjie Zhou, Xiaoying Liu, Jian Ge","doi":"10.1186/s12935-025-03825-8","DOIUrl":"10.1186/s12935-025-03825-8","url":null,"abstract":"<p><strong>Background: </strong>Due to compensatory survival signalling and overexpression of anti-apoptotic Bcl-2 family proteins, the majority of AML patients developed acquired resistance of venetoclax (VEN) to combination therapy of VEN with low-dose cytarabine (LDAC) or hypomethylating agents (HMAs). Dysregulation of the Wnt/β-catenin signalling pathway is intently associated with leukemia development and chemotherapy resistance. However, there is currently no Wnt/β-catenin inhibitor approved for clinical use and it is not clear whether targeting the Wnt/β-catenin pathway enhances the anti-leukemic activity of VEN.</p><p><strong>Methods: </strong>Analysis of the AML patient's data in the BeatAML and GEO databases. Establishing the MOLM13 venetoclax-resistant cell line (MOLM13-R cells) based on the MOLM13 parental cell line. CCK-8, Annexin-V/PI and Western blotting were performed to assess the effects of the combination of Wnt/β-catenin inhibitor C-82 and VEN in AML cell lines. The potential mechanisms of synergistic effects of the two-drug combination were explored by Western blotting and ubiquitination immunoprecipitation.</p><p><strong>Results: </strong>We displayed that the expression of β-catenin abnormally upregulated in AML patients and MOLM13-R cells. Knockdown of β-catenin could increase cell apoptosis in MOLM13-R cells. Combined treatment of C-82 with VEN synergistically inhibited AML cell growth and increased apoptosis. Mechanistically, C-82 disrupted the stability of Mcl-1 protein, and Mcl-1 downregulation was associated with different phosphorylation sites of Mcl-1 and proteasomal degradation. The combination of C-82 and VEN synergistically induced concurrent mitochondrial-associated apoptosis and gasdermin E (GSDME)-dependent pyroptosis.</p><p><strong>Conclusion: </strong>Our findings propose an effective treatment strategy for AML patients through the combination of C-82 and VEN, positioning this regimen as a promising therapeutic option.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"197"},"PeriodicalIF":5.3,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocellular carcinoma drug resistance models.","authors":"Xiaolu Xie, Yaomin Wang, Ziyi Wang, Lei Zhang, Jun Li, Yaling Li","doi":"10.1186/s12935-025-03821-y","DOIUrl":"10.1186/s12935-025-03821-y","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide. Although drug therapy has been well developed and applied, its clinical efficacy is limited due to primary or acquired drug resistance in most HCC patients. Therefore, it is of great clinical significance to elucidate the key molecular mechanisms of resistance and improve the sensitivity of HCC cells to drugs. At present, a variety of HCC drug resistance models have been developed to find out resistance mechanisms, screen biomarkers, and explore strategies to reverse drug resistance, including traditional HCC drug resistance models, HCC patient-derived drug resistance models, three-dimensional drug resistance models, transgenic drug resistance models, and multi-drug resistance models. Here, we searched PubMed, Embase and Web of science for studies related to HCC drug resistance models in recent years, systematically summarized the established methods and characteristics of these models, reviewed their applications and compared their advantages and disadvantages, aiming to provide reference for the selection of appropriate models for HCC drug resistance research.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"195"},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121111/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoprevention of non-viral cancers: challenges and strategies for early intervention.","authors":"Kajal Biswas, Lillian S Kuo, Robert H Shoemaker, Altaf Mohammed","doi":"10.1186/s12935-025-03817-8","DOIUrl":"10.1186/s12935-025-03817-8","url":null,"abstract":"<p><p>While the effects of cancer vaccines have been extensively studied in the therapeutic setting, research has been more limited in the areas of cancer prevention and interception. Although cancer prevention by vaccines has been possible for viral-mediated cancers, such as cervical cancers and hepatocellular carcinoma, preventing non-viral cancers by immunopreventive vaccines is challenging. Many tumors at late stages are less responsive to treatments, including immunotherapies and vaccines, in part due to an immunosuppressive microenvironment. Shifting the strategy to intervention at early stages of cancer development and progression and focusing on high-risk cohorts with defined molecular targets offers a pathway for improved vaccine efficacy. Current research on the role of immune mechanisms during tumor initiation and progression is rapidly evolving and recent emerging preclinical immunoprevention studies have shown that vaccines can induce host immune response and effectively control tumor onset and progression. In this review, we address important considerations and challenges regarding the development of cancer immunoprevention for non-viral cancers. We also discuss significant, innovative, and impactful preclinical and clinical immunoprevention studies in various cancers. This includes neoantigen discovery, the use and optimization of immunomodulating agents either alone or in combination with vaccines, and strategies for optimizing vaccines. We conclude by discussing prospects for immunoprevention research and potential opportunities to advance the field in the future.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"196"},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revealing a novel Decorin-expressing tumor stromal subset in hepatocellular carcinoma via integrative analysis single-cell RNA sequencing.","authors":"Chi Hsiao, Wen-Chieh Liao, Ju-Pi Li, Yu-Cheng Chou, Yu-Lun Chou, Jeng-Rong Lin, Chia-Hua Chen, Chiung-Hui Liu","doi":"10.1186/s12935-025-03811-0","DOIUrl":"10.1186/s12935-025-03811-0","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality, emphasizing the need for novel therapeutic strategies. Decorin (DCN), a chondroitin sulfate proteoglycan (CSPG), has been proposed as a tumor suppressor, yet its precise role in HCC and the tumor microenvironment (TME) remains underexplored. Through integrated analyses of bulk RNA and single-cell RNA sequencing datasets, we identified a distinct tumor stromal subset highly expressing DCN and associated chondroitin sulfate (CS) synthases. Our findings revealed that DCN expression is significantly downregulated in HCC tissue, but upregulated in peri-tumor stroma, where it correlates with better prognosis and reduced capsular invasion. Western blot analysis demonstrated that CS-DCN, the glycosylated form of DCN, plays a dominant role in this context. Single-cell clustering analysis identified a unique stromal subset in HCC characterized by elevated expression of DCN, CSPGs, and CS synthases, associated with extracellular matrix (ECM) remodeling and protective barrier functions. A six-gene DCN-associated signature derived from this subset, including DCN, BGN, SRPX, CHSY3, CHST3, and CHPF, was validated as a prognostic marker for HCC. Furthermore, functional assays demonstrated that CS-DCN significantly inhibited HCC cell proliferation and invasion. Our study highlights the critical role of DCN in HCC TME and provides insights into its therapeutic potential. Modulating CSPG pathways, particularly on CS-DCN-expressing stromal cells, may offer a promising approach for improving HCC treatment and patient outcomes.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"194"},"PeriodicalIF":5.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transforming bone cancer treatment: a comprehensive review of green-synthesized metal nanoparticles.","authors":"Linying Xia, Chao Zhou, Xiankun Liu, Yijun Yu, Qiong Xie, Hongming Lin, Xiaochun Xiong, Songou Zhang, Wenqing Liang, Haiyan Shao","doi":"10.1186/s12935-025-03827-6","DOIUrl":"10.1186/s12935-025-03827-6","url":null,"abstract":"<p><p>Osteosarcoma (OS), chondrosarcoma (CHS), and Ewing sarcoma (EWS) are the main types of bone cancer (BC). OS is the most common BC in this group. It is most common in children and older people, especially in their long bones. Treatments for bone sarcomas and tumors have slowly improved, so researchers began looking into additional and alternative approaches to standard therapies. Therefore, the ability to precisely manipulate metallic nanoparticles (MNPs)' form, size, charge, and surface modification makes them very useful in treating bone cancer. However, due to the biocompatibility and possible toxicity of MNPs, MNP has limits for clinical use in treating BC. Therefore, the green synthesis of MNPs is achieved by bio-reducing metallic ions, which results in the creation of NPs, using living entities or their extracts. Green MNPs derived from natural sources provide a secure and environmentally responsible solution. Benefits of green MNPs include tailored medicine delivery and biocompatibility. Green MNPs reduce damage to healthy cells while improving the targeting of bone cancer cells. In this study, we reviewed how different MNPs synthesized using green methods can help treat various types of BC. This work reviewed the usual way of making MNPs for treating BC, the problems with this standard way of making MNPs, and the benefits and possible future uses of green synthetic MNPs for treating BC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"193"},"PeriodicalIF":5.3,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA16 inhibits pyroptosis and promotes platinum resistance in non-small cell lung cancer by sponging miRNA1827 to regulate MBD3/GSDME expression.","authors":"Yanfang Liu, Yuanjun Zeng, Sikai Wang, Jiangyan Chen, Zhouqi Wang, Yang Zhao, Kuiyu Gong, Guihua Wang","doi":"10.1186/s12935-025-03812-z","DOIUrl":"10.1186/s12935-025-03812-z","url":null,"abstract":"<p><strong>Background: </strong>Platinum-based chemotherapy is the standard first-line cancer treatment. However, patients experience relapses due to chemoresistance. We found that long non-coding RNA 16 (lncRNA16) promotes platinum resistance and inhibits cell death in non-small cell lung cancer (NSCLC). However, the type of cell death inhibited by lncRNA16 remains unknown.</p><p><strong>Methods: </strong>The biological roles of lncRNA16 and microRNA 1827 (miRNA1827) in cell proliferation and colony formation were determined using functional experiments. Dual-luciferase reporter and RNA immunoprecipitation assays were performed to confirm the interactions between lncRNA16 and miRNA1827. In vivo patient-derived tumor xenograft (PDX) models were used to investigate the effects of miRNA1827 agomir on platinum resistance.</p><p><strong>Results: </strong>Pyroptosis was inhibited in platinum-resistant NSCLC cells. LncRNA16 contributed to the expression of methyl-CpG binding domain protein 3 (MBD3) by sponging miRNA1827, thereby inhibiting gasdermin E (GSDME) expression, which inhibited pyroptosis in platinum-resistant NSCLC. The miRNA1827 agomir repressed platinum resistance in vitro experiments and in vivo PDX models.</p><p><strong>Conclusion: </strong>We identified a novel function of lncRNA16 in inhibiting pyroptosis and proposed an effective therapeutic drug, the miRNA1827 agomir, for chemosensitization. This study offers a potential strategy for treating patients with NSCLC, especially those with platinum resistance.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"192"},"PeriodicalIF":5.3,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}