Cancer Cell International最新文献

{"title":"Brachyury promotes proliferation and migration of colorectal cancer cells by targeting MMP14.","authors":"Ming Chen, Huiheng Qu, Xiao Liang, Ying Huang, Zhengjie Yang, Pei Lu, Keqin Shi, Peng Chen, Yanjing Zhang, Hui Zhou, Jiazeng Xia, Jun Shen","doi":"10.1186/s12935-025-03726-w","DOIUrl":"10.1186/s12935-025-03726-w","url":null,"abstract":"<p><strong>Background: </strong>The incidence and mortality rates of colorectal cancer (CRC) are rising, and it is the second most common cause of cancer-related deaths worldwide. Although the transcription factor, Brachyury is intricately linked with various clinical malignancies, the mechanisms by which it influences CRC cell proliferation and migration are inadequately understood.</p><p><strong>Methods: </strong>Tissue microarray was used to evaluate Brachyury expression in CRC and adjacent normal tissues. The effects of Brachyury on HCT116 and SW480 CRC cells were also examined in vitro, including using Cell Counting Kit-8, colony formation, and transwell assays, and in vivo through subcutaneous tumorigenesis assays in a nude mouse xenograft model. Chromatin immunoprecipitation was used to evaluate Brachyury binding to the MMP14 promoter and its impact on MMP14 expression. Rescue experiments were used to elucidate MMP14's role in mediating Brachyury's effect on CRC cell behavior.</p><p><strong>Results: </strong>Brachyury expression was significantly higher in CRC tissues than in adjacent normal tissues, and it promotes CRC oncogenesis in vitro and in vivo. Rescue experiments established MMP14 as a direct, downstream Brachyury target, affirming that MMP14 enhanced Brachyury-driven CRC cell proliferation.</p><p><strong>Conclusion: </strong>Our findings highlight targeting the Brachyury-MMP14 axis as a potential novel approach for CRC clinical therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"132"},"PeriodicalIF":5.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802545","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":"Long noncoding RNAs in acute myeloid leukemia: biomarkers, prognostic indicators, and treatment potential.","authors":"Maryam Farajzadeh, Mehrdad Fathi, Pooya Jalali, Armin Mahmoudsalehi Kheshti, Shahla Khodayari, Mohammad Hojjat-Farsangi, Farhad Jadidi","doi":"10.1186/s12935-025-03763-5","DOIUrl":"10.1186/s12935-025-03763-5","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have been recognized as significant modulators of gene expression and are essential for various biological functions, even though they don't appear to have the ability to encode proteins. Originally considered dark matter, lncRNAs have been recognized as being dysregulated and contributing to the onset, progression, and resistance to treatment of acute myeloid leukemia (AML). AML is a prevalent type of leukemia characterized by the disruption of myeloid cell differentiation, leading to an increased number of immature myeloid progenitor cells. Currently, the need for novel biomarkers and treatment targets to enhance therapeutic alternatives has led to a focus on lncRNAs as possible indicators for prognostic, therapeutic, and diagnostic systems in various human cancers, including AML. Recent research has recognized a limited set of lncRNAs as possible prognostic biomarkers or diagnoses in AML. This review evaluates the key research that highlights the significance of lncRNAs in AML and discusses their roles and impacts on the disease. Furthermore, we intend to underscore the importance of lncRNAs as new and trustworthy markers for the diagnosis, prediction, drug resistance, and targets for treatment in AML.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"131"},"PeriodicalIF":5.3,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787966","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":"Ginger extract inhibits c-MET activation and suppresses osteosarcoma in vitro and in vivo.","authors":"Ruoping Yanzhang, Mingyang Yan, Zhaojie Yang, Huijun Zhang, Yin Yu, Xiangping Li, Ruifang Shen, Xiao Chu, Siyuan Han, Ziliang Zhang, Junyan Teng, Hao Li, Tao Li, Guoguo Jin, Zhiping Guo","doi":"10.1186/s12935-025-03759-1","DOIUrl":"10.1186/s12935-025-03759-1","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma (OS) as an invasive and lethal malignancy showing a low 5-year survival rate requires novel therapeutic targets and their suppressors to improve prevention and treatment strategies.</p><p><strong>Methods: </strong>Our research served to clarify the therapeutic potential of ginger extract and its underlying antineoplastic mechanisms in OS. In vitro studies were used to detect the anti-proliferation ability of ginger extract towards OS cells. Patient-derived xenograft (PDX) was performed to confirm whether ginger extract suppressed tumor growth. Cancer Heat Shock Protein (HSP) database was utilized to identify the potential target of ginger extract, which was subsequently validated through a computational docking model screening method, molecular dynamics simulations and pull-down assay. Analysis of the Gene Expression Omnibus (GEO) database revealed the c-MET expression among OS samples as well as the potential mechanism. Immunohistochemistry (IHC) staining corroborated the c-MET expression level among OS tissues relative to the controls. Functional studies involving c-MET knockdown among OS cell lines were produced to elucidate the functional role of c-MET in OS cellular processes.</p><p><strong>Results: </strong>In vitro studies demonstrated that ginger extract administration impeded OS cell progress while inducing apoptosis and inhibiting migration. Moreover, in vivo tests unveiled that ginger extract prominently inhibited patient-derived xenograft (PDX) tumor development. Cancer HSP database analysis recognized c-MET as an underlying target of ginger extract, which was subsequently validated through a computational docking model screening, molecular dynamics simulations and pull-down assay. Analysis of the Gene Expression Omnibus (GEO) database combined with immunohistochemistry (IHC) staining corroborated the c-MET overexpression among OS tissues in contrast with the controls. Next, our study confirmed the significant suppression of cell progress and anchorage-independent growth, while concomitantly inducing apoptosis after c-MET knockdown, underscoring its prospect for a therapeutic target.</p><p><strong>Conclusion: </strong>Collectively, our findings show that c-MET is a prospective therapeutic target for OS. Ginger extract, a natural c-MET inhibitor, exhibits potent antineoplastic effects by suppressing OS growth both in vitro and in vivo, highlighting its prospect for a new therapeutic agent of this aggressive malignancy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"130"},"PeriodicalIF":5.3,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787962","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":"Heme oxygenase 1 confers gilteritinib resistance in FLT3-ITD acute myeloid leukemia in a STAT6-dependent manner.","authors":"Tianzhuo Zhang, Danna Wei, Yun Zhan, Zhengmei Long, Tingting Lu, Peng Zhao, Rui Gao, Qian Kang, Luxin Zhang, Min Liu, Xueying Yang, Jishi Wang","doi":"10.1186/s12935-025-03757-3","DOIUrl":"10.1186/s12935-025-03757-3","url":null,"abstract":"<p><strong>Background: </strong>Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. We previously discovered that heme oxygenase 1 (HO1) is crucial for chemoresistance in AML, but the detailed molecular mechanism of that remains unclear.</p><p><strong>Methods: </strong>RNA sequencing was conducted to assess transcriptomic changes in three pairs of AML cells after regulating the expression of HO1. The molecular mechanism by which HO1 induces gilteritinib resistance in FLT3-ITD (FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD)) AML was evaluated by quantitative real-time PCR (qRT-PCR), CCK-8, flow cytometry, and western blotting. FLT3-ITD AML mouse models were established to investigate the effects of HO1 expression on gilteritinib resistance in vivo.</p><p><strong>Results: </strong>In these three pairs of AML cells, we discovered that HO1-mediated drug resistance is connected to the interleukin-4-mediated signaling pathway (specifically STAT6) only in MV4-11 cells with the FLT3-ITD mutation. Further findings revealed that HO1 overexpression confers gilteritinib resistance in FLT3-ITD AML cell lines and primary individual specimens. While suppression of HO1 sensitized FLT3-ITD AML cell lines and primary individual specimens to gilteritinib. Mechanistically, western blotting and flow cytometry confirmed that HO1-mediated gilteritinib resistance is related to STAT6 phosphorylation in FLT3-ITD AML cell lines and primary individual specimens. Moreover, tumor-bearing mice were employed to determine that HO1 overexpression conferred gilteritinib resistance in vivo.</p><p><strong>Conclusions: </strong>Collectively, these studies illustrate that HO1 may act as a successful treatment target for gilteritinib-resistant FLT3-ITD AML patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"129"},"PeriodicalIF":5.3,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787964","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":"Pan-cancer analysis identifies CLEC12A as a potential biomarker and therapeutic target for lung adenocarcinoma.","authors":"Desheng Zhou, Yachao Cui, Tianxiang Liang, Zhenpeng Wu, Haiping Yan, Yingchang Li, Wenguang Yin, Yunen Lin, Qiang You","doi":"10.1186/s12935-025-03755-5","DOIUrl":"10.1186/s12935-025-03755-5","url":null,"abstract":"<p><p>C-type lectin domain family 12 member A (CLEC12A) is a type II transmembrane glycoprotein widely expressed in innate immune cells, where it plays a crucial role in immune modulation and has been implicated in cancer progression. However, its precise function in oncogenesis and immune infiltration remains incompletely understood. To investigate this, we utilized multiple databases to assess the mRNA and protein expression levels of CLEC12A across normal tissues and a broad spectrum of cancers. We also evaluated its prognostic and diagnostic significance in pan-cancer contexts. Furthermore, the relationship between CLEC12A expression and immune cell infiltration, immune checkpoints, and immune predictors was explored. In addition, Weighted Gene Co-Expression Network Analysis (WGCNA) and differential expression analysis were performed to examine the biological relevance of CLEC12A in lung adenocarcinoma (LUAD). We also leveraged various databases to predict CLEC12A's response to immunotherapy and drug sensitivity. Finally, in vitro experiments validated the functional role of CLEC12A in LUAD. Our comprehensive pan-cancer analysis revealed that CLEC12A exhibited distinct expression patterns across different cancer types, suggesting its potential as both a diagnostic and prognostic biomarker. Notably, CLEC12A expression was strongly correlated with immune cell infiltration, immune checkpoints, and immune predictors. Functional enrichment analysis highlighted that increased CLEC12A expression in LUAD was associated with a variety of immune-related biological processes and pathways. Moreover, CLEC12A showed significant predictive value for immunotherapy outcomes, and several drugs targeting CLEC12A were identified. In vitro experiments further demonstrated that CLEC12A overexpression inhibited the proliferation, migration, and invasion of LUAD cells. Taken together, our findings position CLEC12A as a promising candidate for cancer detection, prognosis, and as a therapeutic target, particularly in LUAD, where it may serve as a potential target for both immunotherapy and targeted therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"128"},"PeriodicalIF":5.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779219","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":"STAT3/TGFBI signaling promotes the temozolomide resistance of glioblastoma through upregulating glycolysis by inducing cellular senescence.","authors":"Yanbin Zhang, Xiaohua Xiao, Ge Yang, Xiaobing Jiang, Shujie Jiao, Yingli Nie, Tao Zhang","doi":"10.1186/s12935-025-03770-6","DOIUrl":"10.1186/s12935-025-03770-6","url":null,"abstract":"<p><p>Glioblastoma (GBM) is the most lethal type of brain tumor. Recent studies have indicated that cellular senescence-targeted therapy is a promising approach for cancer treatment. However, the underlying mechanisms remain to be clarified. In this study, 101 unique combinations of 10 machine learning algorithms were used to construct prognostic models based on cellular senescence-related genes (CSRGs). We developed the CSRG signature (CSRGS) using machine learning models that exhibited optimal performance. GBM samples were stratified into high- and low-CSRGS groups based on CSRGS scores. Patients in the high-CSRGS group exhibited a worse prognosis, higher immune infiltration, and increased sensitivity to immune checkpoint blockade therapy. Furthermore, senescence-related pathways were significantly correlated with glycolysis, indicating upregulated glycolytic metabolism in senescent GBM cells. We identified TGFBI as a key regulator that played vital roles in both glycolysis and cellular senescence in GBM. TGFBI was overexpressed in GBM samples compared to normal brain tissues, and its knockdown via shRNA inhibited cellular senescence, glycolysis, and temozolomide resistance. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays confirmed that TGFBI is a direct STAT3 target and is required for the STAT3-induced promotion of cellular senescence, glycolysis, and drug resistance. The STAT3-TGFBI axis could be a potential target for senescence-targeted GBM therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"127"},"PeriodicalIF":5.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779220","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":"EIF2S2 as a prognostic marker and therapeutic target in glioblastoma: insights into its role and downstream mechanisms.","authors":"Bo Fan, Qing Pan, Xiaokai Yuan, Wei Du, Zhongjie Yan","doi":"10.1186/s12935-025-03762-6","DOIUrl":"10.1186/s12935-025-03762-6","url":null,"abstract":"<p><p>Glioblastoma (GBM) the most common and most aggressive primary brain tumor has a five-year survival rate of less than 5%. The onset of GBM is very complicated and has always been the focus of researchers. This study analyzed data from 637 GBM and 20 normal tissues from The Cancer Genome Atlas (TCGA), and patients were categorized into high and low EIF2S2 expression groups. The Overall survival and disease-free survival of GBM patients in low expression of EIF2S2 group were significantly higher than those in high expression of EIF2S2 group (p < 0.001), and the expression level of EIF2S2 was significantly correlated with tumor grade (p < 0.001) and tumor recurrence (p < 0.001). The study designed three different short hairpin RNA (shRNA) sequence vectors, identifying shEIF2S2-1 as the most effective. This vector significantly reduced EIF2S2 expression, cell proliferation, and migration while increasing apoptosis in SHG-44 and U251 cells (p < 0.01). By detecting SHG-44 cells infected with shEIF2S2 vector and shCtrl with human whole gene expression chip, we identified WNT5A that is a downstream target gene of EIF2S2. Interfering with WNT5A and overexpressing EIF2S2 in SHG-44 and U251 cells revealed that EIF2S2 regulates WNT5A expression. This regulation led to an increased apoptosis rate (p < 0.05) and a significant reduction in cell migration (p < 0.05) in both the EIF2S2 overexpression and shWNT5A interference groups, confirming that WNT5A is a downstream regulatory target of EIF2S2. This study revealed the key role of EIF2S2 in GBM and its potential molecular mechanism.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"126"},"PeriodicalIF":5.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771506","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":"Regulation of microtubule nucleation in glioblastoma cells by ARF GTPase-activating proteins GIT1 and GIT2 and protein kinase C.","authors":"Vadym Sulimenko, Eduarda Dráberová, Vladimíra Sládková, Tetyana Sulimenko, Věra Vosecká, Omar Skalli, Pavel Dráber","doi":"10.1186/s12935-025-03740-y","DOIUrl":"10.1186/s12935-025-03740-y","url":null,"abstract":"<p><strong>Background: </strong>G protein-coupled receptor kinase-interacting proteins (GITs) function as GTPase-activating proteins (GAPs) for small GTPases of the ADP-ribosylation factor (Arf) family. While GIT proteins (GIT1 and GIT2) regulate both cell migration and microtubule organization, their corresponding regulatory mechanisms in glioblastoma cells remain largely unknown. To further investigate their role in microtubule modulation, we examined the function of GITs in microtubule nucleation and the involvement of protein kinase C (PKC) in this process.</p><p><strong>Methods: </strong>Glioblastoma cell lines with depleted GIT protein levels were generated using shRNA lentiviral vectors. The cellular localization of GITs was visualized by immunofluorescence microscopy, microtubule nucleation was analyzed using time-lapse imaging, and cell migration was assessed through a wound healing assay. Phosphomimetic and non-phosphorylatable variants of GIT2 were prepared by site-directed mutagenesis. Immunoprecipitation, pull-down experiments, and kinase assays in the presence of PKC inhibitors were used to study protein interactions.</p><p><strong>Results: </strong>Both GIT1 and GIT2 associate with proteins of the γ-tubulin ring complexes (γTuRCs), the primary microtubule nucleators, and localize to centrosomes. Depletion of GIT2 enhances centrosomal microtubule nucleation and has a more pronounced, yet opposite, effect on this process compared to GIT1. In contrast, the depletion of both GIT1 and GIT2 similarly affects cell migration. The N-terminal ArfGAP domain of GIT2 associates with centrosomes, regulates microtubule nucleation, and is phosphorylated by PKC, which modulates this process. We identified serine 46 (S46) on the ArfGAP domain as a PKC phosphorylation site and demonstrated that phosphorylation of GIT2 at S46 promotes microtubule nucleation.</p><p><strong>Conclusions: </strong>We propose that GIT2 phosphorylation provides a novel regulatory mechanism for microtubule nucleation in glioblastoma cells, contributing to their invasive properties.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"125"},"PeriodicalIF":5.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771158","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":"Non-coding RNAs, a double-edged sword in breast cancer prognosis.","authors":"Maryam Solaimani, Sahar Hosseinzadeh, Mozhgan Abasi","doi":"10.1186/s12935-025-03679-0","DOIUrl":"10.1186/s12935-025-03679-0","url":null,"abstract":"<p><p>Cancer is a rising issue worldwide, and numerous studies have focused on understanding the underlying reasons for its occurrence and finding proper ways to defeat it. By applying technological advances, researchers are continuously uncovering and updating treatments in cancer therapy. Their vast functions in the regulation of cell growth and proliferation and their significant role in the progression of diseases, including cancer. This review provides a comprehensive analysis of ncRNAs in breast cancer, focusing on long non-coding RNAs such as HOTAIR, MALAT1, and NEAT1, as well as microRNAs such as miR-21, miR-221/222, and miR-155. These ncRNAs are pivotal in regulating cell proliferation, metastasis, drug resistance, and apoptosis. Additionally, we discuss experimental approaches that are useful for studying them and highlight the advantages and challenges of each method. We then explain the results of these clinical trials and offer insights for future studies by discussing major existing gaps. On the basis of an extensive number of studies, this review provides valuable insights into the potential of ncRNAs in cancer therapy. Key findings show that even though the functions of ncRNAs are vast and undeniable in cancer, there are still complications associated with their therapeutic use. Moreover, there is an absence of sufficient experiments regarding their application in mouse models, which is an area to work on. By emphasizing the crucial role of ncRNAs, this review underscores the need for innovative approaches and further studies to explore their potential in cancer therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"123"},"PeriodicalIF":5.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762975","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":"LncRNA SPINT1-AS1 enhances the Warburg effect and promotes the progression of osteosarcoma via the miR-135b-5p/PGAM1 axis.","authors":"Jinyou Wang, Ning Zhang, Yan Wang, Fanghong Chen, Lei Wang, Kailun Wang, Xiao Yao, Xiaohui Pan","doi":"10.1186/s12935-025-03761-7","DOIUrl":"10.1186/s12935-025-03761-7","url":null,"abstract":"<p><p>Osteosarcoma (OS) is a malignant bone tumor that originates from interstitial tissues and affects the health of children and adolescents. Long noncoding RNAs (lncRNAs) are an intriguing category of widely distributed endogenous RNAs involved in OS progression, many of which remain functionally uncharacterized. Herein, we observed an increased expression of lncRNA SPINT1-AS1 in OS tissues and cell lines. Further analysis confirmed that SPINT1-AS1 promotes the proliferation and metastasis of OS cells. Moreover, miR-135b-5p was identified as a downstream target of SPINT1-AS1. Through bioinformatics analysis, PGAM1 mRNA was validated as a target of miR-135b-5p via RIP and luciferase reporter assays. SPINT1-AS1 could enhance OS cell proliferation and metastasis by promoting aerobic glycolysis, acting as a ceRNA by binding to miR-135b-5p, thereby increasing PGAM1 expression. Taken together, these results indicate that SPINT1-AS1 functions as a tumor promoter and regulates OS cell progression through the miR-135b-5p/PGAM1 axis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"124"},"PeriodicalIF":5.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762974","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}