Cancer Biology & Therapy最新文献

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TOP2A modulates signaling via the AKT/mTOR pathway to promote ovarian cancer cell proliferation. TOP2A 通过 AKT/mTOR 通路调节信号,促进卵巢癌细胞增殖。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-06 DOI: 10.1080/15384047.2024.2325126
Kaiwen Zhang, Xingyu Zheng, Yiqing Sun, Xinyu Feng, Xirong Wu, Wenlu Liu, Chao Gao, Ye Yan, Wenyan Tian, Yingmei Wang
{"title":"TOP2A modulates signaling via the AKT/mTOR pathway to promote ovarian cancer cell proliferation.","authors":"Kaiwen Zhang, Xingyu Zheng, Yiqing Sun, Xinyu Feng, Xirong Wu, Wenlu Liu, Chao Gao, Ye Yan, Wenyan Tian, Yingmei Wang","doi":"10.1080/15384047.2024.2325126","DOIUrl":"10.1080/15384047.2024.2325126","url":null,"abstract":"<p><p>Ovarian cancer (OC) is a form of gynecological malignancy that is associated with worse patient outcomes than any other cancer of the female reproductive tract. Topoisomerase II α (TOP2A) is commonly regarded as an oncogene that is associated with malignant disease progression in a variety of cancers, its mechanistic functions in OC have yet to be firmly established. We explored the role of TOP2A in OC through online databases, clinical samples, in vitro and in vivo experiments. And initial analyses of public databases revealed high OC-related TOP2A expression in patient samples that was related to poorer prognosis. This was confirmed by clinical samples in which TOP2A expression was elevated in OC relative to healthy tissue. Kaplan-Meier analyses further suggested that higher TOP2A expression levels were correlated with worse prognosis in OC patients. In vitro, TOP2A knockdown resulted in the inhibition of OC cell proliferation, with cells entering G1 phase arrest and undergoing consequent apoptotic death. In rescue assays, TOP2A was confirmed to regulate cell proliferation and cell cycle through AKT/mTOR pathway activity. Mouse model experiments further affirmed the key role that TOP2A plays as a driver of OC cell proliferation. These data provide strong evidence supporting TOP2A as an oncogenic mediator and prognostic biomarker related to OC progression and poor outcomes. At the mechanistic level, TOP2A can control tumor cell growth via AKT/mTOR pathway modulation. These preliminary results provide a foundation for future research seeking to explore the utility of TOP2A inhibitor-based combination treatment regimens in platinum-resistant recurrent OC patients.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038743","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}
引用次数: 0
Efficacy and pharmacodynamic effect of anti-CD73 and anti-PD-L1 monoclonal antibodies in combination with cytotoxic therapy: observations from mouse tumor models. 抗CD73和抗PD-L1单克隆抗体联合细胞毒疗法的疗效和药效学效应:小鼠肿瘤模型观察。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-01-11 DOI: 10.1080/15384047.2023.2296048
Brajesh P Kaistha, Gozde Kar, Andreas Dannhorn, Amanda Watkins, Grace Opoku-Ansah, Kristina Ilieva, Stefanie Mullins, Judith Anderton, Elena Galvani, Fabien Garcon, Jean-Martin Lapointe, Lee Brown, James Hair, Tim Slidel, Nadia Luheshi, Kelli Ryan, Elizabeth Hardaker, Simon Dovedi, Rakesh Kumar, Robert W Wilkinson, Scott A Hammond, Jim Eyles
{"title":"Efficacy and pharmacodynamic effect of anti-CD73 and anti-PD-L1 monoclonal antibodies in combination with cytotoxic therapy: observations from mouse tumor models.","authors":"Brajesh P Kaistha, Gozde Kar, Andreas Dannhorn, Amanda Watkins, Grace Opoku-Ansah, Kristina Ilieva, Stefanie Mullins, Judith Anderton, Elena Galvani, Fabien Garcon, Jean-Martin Lapointe, Lee Brown, James Hair, Tim Slidel, Nadia Luheshi, Kelli Ryan, Elizabeth Hardaker, Simon Dovedi, Rakesh Kumar, Robert W Wilkinson, Scott A Hammond, Jim Eyles","doi":"10.1080/15384047.2023.2296048","DOIUrl":"10.1080/15384047.2023.2296048","url":null,"abstract":"<p><p>CD73 is a cell surface 5'nucleotidase (NT5E) and key node in the catabolic process generating immunosuppressive adenosine in cancer. Using a murine monoclonal antibody surrogate of Oleclumab, we investigated the effect of CD73 inhibition in concert with cytotoxic therapies (chemotherapies as well as fractionated radiotherapy) and PD-L1 blockade. Our results highlight improved survival in syngeneic tumor models of colorectal cancer (CT26 and MC38) and sarcoma (MCA205). This therapeutic outcome was in part driven by cytotoxic CD8 T-cells, as evidenced by the detrimental effect of CD8 depleting antibody treatment of MCA205 tumor bearing mice treated with anti-CD73, anti-PD-L1 and 5-Fluorouracil+Oxaliplatin (5FU+OHP). We hypothesize that the improved responses are tumor microenvironment (TME)-driven, as suggested by the lack of anti-CD73 enhanced cytopathic effects mediated by 5FU+OHP on cell lines <i>in vitro</i>. Pharmacodynamic analysis, using imaging mass cytometry and RNA-sequencing, revealed noteworthy changes in specific cell populations like cytotoxic T cells, B cells and NK cells in the CT26 TME. Transcriptomic analysis highlighted treatment-related modulation of gene profiles associated with an immune response, NK and T-cell activation, T cell receptor signaling and interferon (types 1 & 2) pathways. Inclusion of comparator groups representing the various components of the combination allowed deconvolution of contribution of the individual therapeutic elements; highlighting specific effects mediated by the anti-CD73 antibody with respect to immune-cell representation, chemotaxis and myeloid biology. These pre-clinical data reflect complementarity of adenosine blockade with cytotoxic therapy, and T-cell checkpoint inhibition, and provides new mechanistic insights in support of combination therapy.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10793677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139416454","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}
引用次数: 0
Correction. 更正。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-15 DOI: 10.1080/15384047.2024.2352926
{"title":"Correction.","authors":"","doi":"10.1080/15384047.2024.2352926","DOIUrl":"https://doi.org/10.1080/15384047.2024.2352926","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140944101","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}
引用次数: 0
Correction. 更正。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-01 DOI: 10.1080/15384047.2024.2375109
{"title":"Correction.","authors":"","doi":"10.1080/15384047.2024.2375109","DOIUrl":"10.1080/15384047.2024.2375109","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476013","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}
引用次数: 0
miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2. miR-10b-5p 通过靶向 SLC38A2 调节肝癌细胞代谢促进肿瘤生长
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-23 DOI: 10.1080/15384047.2024.2315651
Mingzhi Xia, Jie Chen, Yingyun Hu, Bin Qu, Qianqian Bu, Haoming Shen
{"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":null,"pages":null},"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}
引用次数: 0
MiR-378a-5p exerts a radiosensitizing effect on CRC through LRP8/β-catenin axis. MiR-378a-5p通过LRP8/β-catenin轴对CRC产生放射增敏作用。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-22 DOI: 10.1080/15384047.2024.2308165
Guolin Hu, Pengbiao Che, Ling Deng, Lei Liu, Jia Liao, Qi Liu
{"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":null,"pages":null},"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}
引用次数: 0
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. CD46和CD59抑制剂能增强抗CD38单克隆抗体daratumumab和isatuximab对多发性骨髓瘤和其他B细胞恶性肿瘤细胞的补体依赖性细胞毒性。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-15 DOI: 10.1080/15384047.2024.2314322
Hongjie Wang, Theo Koob, Jonathan R Fromm, Ajay Gopal, Darrick Carter, André Lieber
{"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<sup>high</sup>/CD59<sup>high</sup> 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":null,"pages":null},"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}
引用次数: 0
Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy. 骨髓脂肪细胞在 B 细胞急性淋巴细胞白血病中的动态演变:从诊断到化疗后的启示。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-11 DOI: 10.1080/15384047.2024.2323765
Xi Jia, Naying Liao, Yunqian Yao, Xutao Guo, Kai Chen, Pengcheng Shi
{"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":null,"pages":null},"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}
引用次数: 0
eIf3a mediates malignant biological behaviors in colorectal cancer through the PI3K/AKT signaling pathway. eIf3a 通过 PI3K/AKT 信号通路介导结直肠癌的恶性生物学行为。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-23 DOI: 10.1080/15384047.2024.2355703
Chao Huo, Disheng Wu, Xiaodan Li, Yan Zhang, Baoguang Hu, Taoming Zhang, Jianwei Ren, Tianbao Wang, Yi Liu
{"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":null,"pages":null},"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}
引用次数: 0
Circ_RPPH1 facilitates progression of breast cancer via miR-1296-5p/TRIM14 axis. Circ_RPPH1 通过 miR-1296-5p/TRIM14 轴促进乳腺癌的进展。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-30 DOI: 10.1080/15384047.2024.2360768
Jing Jiang, Shenghong Shi, Wei Zhang, Chao Li, Long Sun, Qidong Ge, Xujun Li
{"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":null,"pages":null},"PeriodicalIF":3.6,"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}
引用次数: 0
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