Cancer Biology & Therapy最新文献

{"title":"Tumor microenvironment in primary central nervous system lymphoma (PCNSL).","authors":"Qiqi Jin, Haoyun Jiang, Ye Han, Litian Zhang, Cuicui Li, Yurong Zhang, Ye Chai, Pengyun Zeng, Lingling Yue, Chongyang Wu","doi":"10.1080/15384047.2024.2425131","DOIUrl":"10.1080/15384047.2024.2425131","url":null,"abstract":"<p><p>Primary central nervous system lymphoma (PCNSL) is one of the rare lymphomas limited to the central nervous system. With the availability of immunotherapy, the tumor microenvironment (TME) attracts much attention nowadays. However, the systematic studies on the TME of PCNSL are lacking. By reviewing the existing research, we found that the TME of PCNSL is infiltrated with abundant TAMs and TILs, among which cytotoxic T cells (CTLs) and M2-polarized macrophages are principal. However, the counts of immune cells infiltrated in the TME of PCNSL are significantly lower than systemic diffuse large B-cell lymphoma (DLBCL). In addition, PCNSL can attract the infiltration of immunosuppressive cells and the loss of HLA I/II expression, overexpress inhibitory immune checkpoints, and release immunosuppressive cytokines to form an immunosuppressive TME. The immunosuppressive effect of TME in PCNSL is significantly stronger than that in systemic DLBCL. These characteristics of TME highlight the immunosuppression of PCNSL.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2425131"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting autophagy promotes the antitumor effect of radiotherapy on cervical cancer cells.","authors":"Fanjie Meng, Ying Yan, Li Zhou, Song Zhao, Lingyan Sun, Huiying Yu","doi":"10.1080/15384047.2024.2431136","DOIUrl":"10.1080/15384047.2024.2431136","url":null,"abstract":"<p><p>Radiotherapy is the mainstay of cancer treatment, and reducing radioresistance is still a poorly explored issue in radiotherapy. Our study was designed to explore the possible functions and mechanisms of autophagy in cervical cancer cells treated with radiotherapy. We discovered that autophagy was activated in C33a and HeLa cervical cancer cells in parallel with increased apoptosis and formation of polyploid giant carcinoma cells (PGCCs) after radiation. Inhibition of autophagy significantly enhances radiation-induced cytotoxicity and apoptosis in cervical cancer cells and reduces PGCCs formation. Immunoblot analysis, as part of the mechanistic experiments, showed that the phosphorylation levels of Akt, mTOR, and P70S6K were downregulated. Thus, our research demonstrated that inhibiting autophagy enhances the antitumor effects of radiation on cervical cancer cells.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2431136"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer.","authors":"Celina Ablinger, Daniel Neureiter, Theresa Mähr, Christian Mayr, Tobias Kiesslich, Nicole Maeding, Irina Valenta, Maximilian Ardelt, Fabian Wilhelm, Elen Neureiter, Markus Ritter, Johanna Pachmayr, Petra Huber-Cantonati","doi":"10.1080/15384047.2024.2439057","DOIUrl":"https://doi.org/10.1080/15384047.2024.2439057","url":null,"abstract":"<p><p>Biliary tract cancer (BTC) is a rare malignancy with rising incidence. The therapeutic options are limited and the overall survival remains poor. Cyclin-dependent kinases, drivers of cell cycle and transcription have numerous biological functions and are known to be dysregulated in numerous tumor entities. Dinaciclib is a selective Cdk1/2/5/9 inhibitor with anti-tumor activity. In the present study, the efficacy of dinaciclib was tested on a comprehensive BTC cell-line model. The results indicate a heterogeneous expression pattern of Cdk1/2/5/9, as well as various differentiation tumor markers in BTC cells. We demonstrated that dinaciclib reduces cell viability, ATP levels, and proliferation rates. Moreover, dinaciclib induces apoptosis via increased caspase 3/7 activity and reduced expression levels of the anti-apoptotic protein Mcl-1 in a concentration- and cell line -dependent manner. 3D cell culture confirms the cytotoxic impact of dinaciclib under more physiologic tumor conditions. Additionally, dinaciclib affects different cell growth regulators like EGFR and STAT3 on gene and protein level, thus decreasing tumor growth. In summary, our study indicates that dinaciclib acts as a promising anti-tumorigenic agent in 2D and 3D <i>in vitro</i> BTC models and thus encourages further investigation.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2439057"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817426","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":"miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2.","authors":"Mingzhi Xia, Jie Chen, Yingyun Hu, Bin Qu, Qianqian Bu, Haoming Shen","doi":"10.1080/15384047.2024.2315651","DOIUrl":"10.1080/15384047.2024.2315651","url":null,"abstract":"<p><p>Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography - mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC <i>in vivo</i>. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2315651"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-378a-5p exerts a radiosensitizing effect on CRC through LRP8/β-catenin axis.","authors":"Guolin Hu, Pengbiao Che, Ling Deng, Lei Liu, Jia Liao, Qi Liu","doi":"10.1080/15384047.2024.2308165","DOIUrl":"10.1080/15384047.2024.2308165","url":null,"abstract":"<p><strong>Background: </strong>MiRNAs are closely related to tumor radiosensitivity. MiR-378a-5p level is down-regulated in colorectal cancer (CRC). Therefore, this study intends to explore the role of miR-378a-5p in CRC, especially radiosensitivity.</p><p><strong>Methods: </strong>The expression of miR-378a-5p was analyzed in CRC samples. CRC cell lines were treated with different doses of X-rays. Bioinformatics analysis, dual-luciferase reporter assay and RT-qPCR were used to detect the expressions and binding relationship of miR-378a-5p and low-density lipoprotein receptor-related protein 8 (LRP8). MiR-378a-5p inhibitor or/and siLRP8 were transfected into CRC cells with or without irradiation. Subsequently, clonogenic assay, flow cytometry and <i>in vivo</i> experiments including tumorigenesis assay, immunohistochemistry, RT-qPCR and Western blot were performed to clarify the role of miR-378a-5p/LRP8 axis in the radiosensitivity of CRC.</p><p><strong>Results: </strong>The down-regulated expression of miR-378a-5p in CRC is related to histological differentiation and tumor-node-metastasis (TNM) stage. After irradiation, the survival fraction of CRC cells was decreased, while the apoptotic rate and the level of miR-378a-5p were increased. Restrained miR-378a-5p repressed apoptosis and apoptosis-related protein expressions, yet promoted the proliferation and the radioresistance of cells by regulating β-catenin in CRC cells. LRP8 was highly expressed in CRC, and targeted by miR-378a-5p. SiLRP8 improved radiosensitivity and reversed the effect of miR-378a-5p down-regulation on CRC cells. Overexpressed miR-378a-5p and irradiation enhanced the level of miR-378a-5p, yet suppressed the expressions of Ki67 and LRP8 as well as tumorigenesis.</p><p><strong>Conclusion: </strong>MiR-378a-5p may exert a radiosensitizing effect on CRC through the LRP8/β-catenin axis, which may be a new therapeutic target for CRC radioresistance.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2308165"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A positive feedback loop of SRSF9/USP22/ZEB1 promotes the progression of ovarian cancer.","authors":"Jing Wang, Ming Hu, Jie Min, Xin Li","doi":"10.1080/15384047.2024.2427415","DOIUrl":"10.1080/15384047.2024.2427415","url":null,"abstract":"<p><p>Ovarian cancer (OC) is recognized as the most lethal type of gynecological malignancy, making treatment options challenging. Discovering novel therapeutic targets will benefit OC patients. This study aimed to reveal the mechanism by which SRSF9 regulates OC progression. Cell proliferation was determined via CCK-8 assays, whereas cell migration and invasion were monitored via Transwell assays. Western blotting and qPCR assays were used to detect protein and mRNA alterations. RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were performed to investigate the relationships between SRSF9 and USP22. Co-IP was used to validate the interaction between USP22 and ZEB1. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were used to verify the regulatory effect of ZEB1 on the transcription of SRSF9. Subcutaneous xenograft models were established to evaluate the impact of SRSF9 on tumor development. Knockdown of SRSF9 significantly suppressed the proliferation, invasion, migration, tumorigenicity, and epithelial‒mesenchymal transition (EMT) of OC cells. SRSF9 can bind to USP22 mRNA, increasing its stability. Moreover, the overexpression of USP22 reversed the impact of SRSF9 silencing on malignant phenotypes. USP22 can mediate the deubiquitination of ZEB1, thereby enhancing the progression of OC. Furthermore, ZEB1 upregulated SRSF9 expression through transcriptional activation, thus establishing a positive feedback loop. SRSF9 enhanced the malignant characteristics of OC through a positive feedback loop of SRSF9/USP22/ZEB1. This functional circuit may help in the development of novel therapeutic approaches for treating OC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2427415"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11559372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy.","authors":"Xi Jia, Naying Liao, Yunqian Yao, Xutao Guo, Kai Chen, Pengcheng Shi","doi":"10.1080/15384047.2024.2323765","DOIUrl":"10.1080/15384047.2024.2323765","url":null,"abstract":"<p><p>Adipocyte is a unique and versatile component of bone marrow microenvironment (BMM). However, the dynamic evolution of Bone Marrow (BM) adipocytes from the diagnosis of B cell Acute Lymphoblastic Leukemia (B-ALL) to the post-treatment state, and how they affect the progression of leukemia, remains inadequately explicated. Primary patient-derived xenograft models (PDXs) and stromal cell co-culture system are employed in this study. We show that the dynamic evolution of BM adipocytes from initial diagnosis of B-ALL to the post-chemotherapy phase, transitioning from cellular depletion in the initial leukemia niche to a fully restored state upon remission. Increased BM adipocytes retards engraftment of B-ALL cells in PDX models and inhibits cells growth of B-ALL in vitro. Mechanistically, the proliferation arrest of B-ALL cells in the context of adipocytes-enrichment niche, might attribute to the presence of adiponectin secreted by adipocytes themselves and the absence of cytokines secreted by mesenchymal stem cell (MSCs). In summary, our findings offer a novel perspective for further in-depth understanding of the dynamic balance between BMM and B-ALL.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2323765"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD46 and CD59 inhibitors enhance complement-dependent cytotoxicity of anti-CD38 monoclonal antibodies daratumumab and isatuximab in multiple myeloma and other B-cell malignancy cells.","authors":"Hongjie Wang, Theo Koob, Jonathan R Fromm, Ajay Gopal, Darrick Carter, André Lieber","doi":"10.1080/15384047.2024.2314322","DOIUrl":"10.1080/15384047.2024.2314322","url":null,"abstract":"<p><p>Multiple myeloma (MM) is an incurable malignancy of the B-cell lineage. Remarkable progress has been made in the treatment of MM with anti-CD38 monoclonal antibodies such as daratumumab and isatuximab, which can kill MM cells by inducing complement-dependent cytotoxicity (CDC). We showed that the CDC efficacy of daratumumab and isatuximab is limited by membrane complement inhibitors, including CD46 and CD59, which are upregulated in MM cells. We recently developed a small recombinant protein, Ad35K++, which is capable of transiently removing CD46 from the cell surface. We also produced a peptide inhibitor of CD59 (rILYd4). In this study, we tested Ad35K++ and rILYd4 in combination with daratumumab and isatuximab in MM cells as well as in cells from two other B-cell malignancies. We showed that Ad35K++ and rILYd4 increased CDC triggered by daratumumab and isatuximab. The combination of both inhibitors had an additive effect <i>in vitro</i> in primary MM cells as well as <i>in vivo</i> in a mouse xenograft model of MM. Daratumumab and isatuximab treatment of MM lines (without Ad35K++ or rILYd4) resulted in the upregulation of CD46/CD59 and/or survival of CD46^high/CD59^high MM cells that escaped the second round of daratumumab and isatuximab treatment. The escape in the second treatment cycle was prevented by the pretreatment of cells with Ad35K++. Overall, our data demonstrate that Ad35K++ and rILYd4 are efficient co-therapeutics of daratumumab and isatuximab, specifically in multi-cycle treatment regimens, and could be used to improve treatment of multiple myeloma.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2314322"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10877974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139740422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"eIf3a mediates malignant biological behaviors in colorectal cancer through the PI3K/AKT signaling pathway.","authors":"Chao Huo, Disheng Wu, Xiaodan Li, Yan Zhang, Baoguang Hu, Taoming Zhang, Jianwei Ren, Tianbao Wang, Yi Liu","doi":"10.1080/15384047.2024.2355703","DOIUrl":"10.1080/15384047.2024.2355703","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is among the most common gastrointestinal malignancies worldwide. eIF3a is highly expressed in a variety of cancer types, yet its role in CRC remains unclear. We introduced ectopic eIF3a expression in CRC cells to investigate its relevance to various malignant behaviors. Further, we silenced eIF3a to explore its effect on tumor growth in a nude mouse tumor xenograft model. Finally, the molecular mechanisms through which eIF3a regulates malignancy in CRC cells were explored through bioinformatics analysis combined with the use of a specific PI3K inhibitor (LY294002). eIF3a was highly expressed in the peripheral blood and cancer tissue of CRC patients. Malignancy and tumor growth were significantly inhibited by silencing eIF3a, while overexpression promoted malignant behaviors, with a positive correlation between PI3K/AKT activation and eIF3a expression. Taken together, eIF3a plays an oncogenic role in CRC by regulating PI3K/AKT signaling and is a potential biomarker for CRC diagnosis and prognostic monitoring.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2355703"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11123456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_RPPH1 facilitates progression of breast cancer via miR-1296-5p/TRIM14 axis.","authors":"Jing Jiang, Shenghong Shi, Wei Zhang, Chao Li, Long Sun, Qidong Ge, Xujun Li","doi":"10.1080/15384047.2024.2360768","DOIUrl":"10.1080/15384047.2024.2360768","url":null,"abstract":"<p><p><i>Circular RNA Ribonuclease P</i> <i>RNA Component H1</i> (<i>circ_RPPH1</i>) and microRNA (miRNA) <i>miR-1296-5p</i> play a crucial role in breast cancer (BC), but the molecular mechanism is vague. Evidence showed that <i>miR-1296-5p</i> can activate <i>tripartite motif-containing 14</i> (<i>TRIM14</i>). Clinical indications of eighty BC patients were collected and the <i>circ_RPPH1</i> expression was detected using real-time quantitative PCR. MCF-7 and MDA-MB-231 cells were transfected with overexpression or knockdown of <i>circ_RPPH1</i>, <i>miR-1296-5p</i>, or <i>TRIM14</i>. Cell counting kit-8, cell cloning formation, wound healing, Transwell, and flow cytometry assays were performed to investigate the malignant phenotype of BC. The dual-luciferase reporter gene analyses were applied to reveal the interaction between these target genes. Subcutaneous tumorigenic model mice were established with <i>circ_RPPH1</i> overexpression MDA-MB-231 cells in vivo; the tumor weight and volume, levels of <i>miR-1296-5</i> and <i>TRIM14</i> mRNA were measured. Western blot and immunohistochemistry were used to detect TRIM14 in cells and mice. <i>Circ_RPPH1</i> levels were notably higher in BC patients and have been found to promote cell proliferation, invasion, and migration of BC cells. <i>Circ_RPPH1</i> altered cell cycle and hindered apoptosis. <i>Circ_RPPH1</i> knockdown or <i>miR-1296-5p</i> overexpression inhibited the malignant phenotype of BC. Furthermore, <i>miR-1296-5p</i> knockdown reversed <i>circ_RPPH1</i>'s promotion effects on BC. Interestingly, <i>TRIM14</i> overexpression counteracts the inhibitory effects of <i>miR-1296-5p</i> overexpression and <i>circ_RPPH1</i> silencing on BC. Moreover, in BC tumor-bearing mice, <i>circ_RPPH1</i> overexpression led to increased TRIM14 expression and facilitated tumor growth. <i>Circ_RPPH1</i> enhanced BC progression through <i>miR-1296-5p</i>/<i>TRIM14</i> axis, indicating its potential as a biomarker and therapeutic target in BC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2360768"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11141472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}