Cancer Biology & Therapy最新文献_第8页

Evaluating massage therapy for radiation-induced fibrosis in rats: preliminary findings and palpation results. 评估按摩疗法对大鼠放射性纤维化的影响：初步发现和触诊结果。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-12-02 DOI: 10.1080/15384047.2024.2436694

Geoffrey M Bove, Holly McMillan, Mary F Barbe

{"title":"Evaluating massage therapy for radiation-induced fibrosis in rats: preliminary findings and palpation results.","authors":"Geoffrey M Bove, Holly McMillan, Mary F Barbe","doi":"10.1080/15384047.2024.2436694","DOIUrl":"10.1080/15384047.2024.2436694","url":null,"abstract":"Radiation-induced fibrosis (RIF) is a common side effect of cancer treatment, but can manifest into a devastating syndrome for which there is no preventive measure or cure. In rats who perform a repetitive work task, who left untreated develop signs and symptoms that resemble repetitive motion disorders in humans, we have shown that manual therapy prevents the development of fibrosis and other key biomarkers. The fibrosis of RIF and repetitive motion disorders has similar biomarkers. In rats, we sought to determine if manual therapy would alter key biomarkers of post-irradiation fibrosis following X-ray irradiation given to the rat forelimb. One limb of rats was given a damaging dose of X-ray irradiation. Some limbs were massaged using a protocol previously described and characterized. Serum inflammatory markers, histological assays of tissue fibrosis and nerve pathology, and electrophysiology for neuropathic discharge were assayed after 8 weeks. We also tested if an experienced therapist could identify the irradiated limb using blinded palpation at the 8 week end-point. While preliminary assays showed robust changes compared to control limbs, the other assays did not show similar pathology. Our therapist could detect each irradiated limb. Serum inflammatory markers were reduced by massage to the irradiated limb. We conclude that blinded palpation is sensitive to detect subtle changes in tissue following irradiation. In contrast to the preliminary studies, the dose of irradiation used was insufficient to induce long-lasting deep fibrosis or nerve degeneration. We suspect that a difference in housing, and thus physical activity, was the plausible reason for this difference.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2436694"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766511","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

Role and mechanism of COL3A1 in regulating the growth, metastasis, and drug sensitivity in cisplatin-resistant non-small cell lung cancer cells. COL3A1在调节顺铂耐药非小细胞肺癌细胞的生长、转移和药物敏感性中的作用和机制

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-26 DOI: 10.1080/15384047.2024.2328382

Jiankun Ren, Songwei Zhao, Junyu Lai

{"title":"Role and mechanism of COL3A1 in regulating the growth, metastasis, and drug sensitivity in cisplatin-resistant non-small cell lung cancer cells.","authors":"Jiankun Ren, Songwei Zhao, Junyu Lai","doi":"10.1080/15384047.2024.2328382","DOIUrl":"10.1080/15384047.2024.2328382","url":null,"abstract":"Non-small cell lung cancer (NSCLC) is among the most difficult malignancies to treat. Type III collagen (COL3A1) can affect the progression and chemoresistance development of NSCLC. We herein explored the mechanism that drives COL3A1 dysregulation in NSCLC. Potential RNA-binding proteins (RBPs) and transcription factors (TFs) that could bind to COL3A1 were searched by bioinformatics. mRNA expression was detected by quantitative PCR. Protein expression was evaluated using immunoblotting and immunohistochemistry. The effects of the variables were assessed by gauging cell growth, invasiveness, migratory capacity, apoptosis, and cisplatin (DDP) sensitivity. The direct YY1/COL3A1 relationship was confirmed by ChIP and luciferase reporter experiments. Xenograft experiments were done to examine COL3A1's function in DDP efficacy. COL3A1 showed enhanced expression in DDP-resistant NSCLC. In H460/DDP and A549/DDP cells, downregulation of COL3A1 exerted inhibitory functions in cell growth, invasiveness, and migration, as well as promoting effects on cell DDP sensitivity and apoptosis. Mechanistically, ELAV-like RNA binding protein 1 (ELAVL1) enhanced the mRNA stability and expression of COL3A1, and Yin Yang 1 (YY1) promoted the transcription and expression of COL3A1. Furthermore, upregulation of COL3A1 reversed ELAVL1 inhibition- or YY1 deficiency-mediated functions in DDP-resistant NSCLC cells. Additionally, COL3A1 downregulation enhanced the anti-tumor efficacy of DDP in vivo. Our investigation demonstrates that COL3A1 upregulation, induced by both RBP ELAVL1 and TF YY1, exerts important functions in phenotypes of NSCLC cells with DDP resistance, offering an innovative opportunity in the treatment of drug-resistant NSCLC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2328382"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10968311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140287029","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

MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells by binding ITGB4/LAMB3 to activate the AKT signaling pathway. MDFI 通过结合 ITGB4/LAMB3 激活 AKT 信号通路，促进结直肠癌细胞的增殖和对化疗的耐受性。

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-20 DOI: 10.1080/15384047.2024.2314324

Ding Ma, Shuwen Liu, Kua Liu, Lingkai Kong, Lingjun Xiao, Qilei Xin, Chunping Jiang, Junhua Wu

{"title":"MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells by binding ITGB4/LAMB3 to activate the AKT signaling pathway.","authors":"Ding Ma, Shuwen Liu, Kua Liu, Lingkai Kong, Lingjun Xiao, Qilei Xin, Chunping Jiang, Junhua Wu","doi":"10.1080/15384047.2024.2314324","DOIUrl":"10.1080/15384047.2024.2314324","url":null,"abstract":"Colorectal cancer (CRC) is one of the most lethal cancers. Single-cell RNA sequencing (scRNA-seq) and protein-protein interactions (PPIs) have enabled the systematic study of CRC. In our research, the activation of the AKT pathway in CRC was analyzed by KEGG using single-cell sequencing data from the GSE144735 dataset. The correlation and PPIs of MDFI and ITGB4/LAMB3 were examined. The results were verified in the TCGA and CCLE and further tested by coimmunoprecipitation experiments. The effect of MDFI on the AKT pathway via ITGB4/LAMB3 was validated by knockdown and lentiviral overexpression experiments. The effect of MDFI on oxaliplatin/fluorouracil sensitivity was probed by colony formation assay and CCK8 assay. We discovered that MDFI was positively associated with ITGB4/LAMB3. In addition, MDFI was negatively associated with oxaliplatin/fluorouracil sensitivity. MDFI upregulated the AKT pathway by directly interacting with LAMB3 and ITGB4 in CRC cells, and enhanced the proliferation of CRC cells via the AKT pathway. Finally, MDFI reduced the sensitivity of CRC cells to oxaliplatin and fluorouracil. In conclusion, MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells, partially through the activation of the AKT signaling pathway by the binding to ITGB4/LAMB3. Our findings provide a possible molecular target for CRC therapy.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2314324"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905144","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

Establishment of a visualized mouse orthotopic xenograft model of nasopharyngeal carcinoma. 建立鼻咽癌可视化小鼠正位异种移植模型。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-29 DOI: 10.1080/15384047.2024.2382531

Wei Chen, Wei-Min Chen, Si-Xia Chen, Li Jiang, Ge-Ge Shu, Yuan-Xiu Yin, Zhi-Peng Quan, Zi-Yan Zhou, Ming-Jun Shen, Ya-Ting Qin, Chao-Lin Yang, Xue-Jin Su, Min Kang

{"title":"Establishment of a visualized mouse orthotopic xenograft model of nasopharyngeal carcinoma.","authors":"Wei Chen, Wei-Min Chen, Si-Xia Chen, Li Jiang, Ge-Ge Shu, Yuan-Xiu Yin, Zhi-Peng Quan, Zi-Yan Zhou, Ming-Jun Shen, Ya-Ting Qin, Chao-Lin Yang, Xue-Jin Su, Min Kang","doi":"10.1080/15384047.2024.2382531","DOIUrl":"10.1080/15384047.2024.2382531","url":null,"abstract":"Mouse orthotopic xenograft tumor models are commonly employed in studies investigating the mechanisms underlying the development and progression of tumors and their preclinical treatment. However, the unavailability of mature and visualized orthotopic xenograft models of nasopharyngeal carcinoma limits the development of treatment strategies for this cancer. The aim of this study was to provide a simple and reliable method for building an orthotopic xenograft model of nasopharyngeal carcinoma. Human nasopharyngeal carcinoma (C666-1-luc) cells, stably expressing the firefly luciferase gene, were injected subcutaneously into the right axilla of BALB/C nude mice. Four weeks later, the resulting subcutaneous tumors were cut into small blocks and grafted into the nasopharynx of immunodeficient BALB/C nude mice to induce tumor formation. Tumor growth was monitored by bioluminescence imaging and small animal magnetic resonance imaging (MRI). The expression of histological and immunological antigens associated with orthotopic xenograft nasopharyngeal carcinoma was analyzed by tissue section analysis and immunohistochemistry (IHC). A visualized orthotopic xenograft nasopharyngeal carcinoma model was successfully developed in this study. Luminescence signal detection, micro-MRI, and hematoxylin and eosin staining revealed the successful growth of tumors in the nasopharynx of the nude mice. Moreover, IHC analysis detected cytokeratin (CK), CK5/6, P40, and P63 expression in the orthotopic tumors, consistent with the reported expression of these antigens in human nasopharyngeal tumors. This study established a reproducible, visual, and less lethal orthotopic xenograft model of nasopharyngeal carcinoma, providing a platform for preclinical research.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2382531"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104699","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

HSPB8-BAG3 chaperone complex modulates cell invasion in intrahepatic cholangiocarcinoma by regulating CASA-mediated Filamin A degradation. HSPB8-BAG3伴侣复合物通过调节CASA介导的Filamin A降解来调节肝内胆管癌的细胞侵袭。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-31 DOI: 10.1080/15384047.2024.2396694

Bo Shu, Yu Wen, Ronghua Lin, Chao He, Cailan Luo, Fazhao Li

{"title":"HSPB8-BAG3 chaperone complex modulates cell invasion in intrahepatic cholangiocarcinoma by regulating CASA-mediated Filamin A degradation.","authors":"Bo Shu, Yu Wen, Ronghua Lin, Chao He, Cailan Luo, Fazhao Li","doi":"10.1080/15384047.2024.2396694","DOIUrl":"10.1080/15384047.2024.2396694","url":null,"abstract":"The incidence of intrahepatic cholangiocarcinoma (ICC) is steadily rising, and it is associated with a high mortality rate. Clinical samples were collected to detect the expression of HSPB8 and BAG3 in ICC tissues. ICC cells were cultured and transfected with plasmids that overexpressed or silenced specific genes to investigate the impact of gene expression alterations on cell function. qPCR and Western blot techniques were utilized to measure gene and protein expression levels. A wound healing assay was conducted to assess cell migration ability. The Transwell assay was used to assess cell invasion ability. Co-IP was used to verify the binding relationship between HSPB8 and BAG3. The effects of HSPB8 and BAG3 on lung metastasis of tumors in vivo were verified by constructing a metastatic tumor model. Through the above experiments, we discovered that the expressions of HSPB8 and BAG3 were up-regulated in ICC tissues and cells, and their expressions were positively correlated. The metastatic ability of ICC cells could be promoted or inhibited by upregulating or downregulating the expression of BAG3. Furthermore, the HSPB8-BAG3 chaperone complex resulted in the abnormal degradation of Filamin A by activating autophagy. Increased expression of Filamin A inhibits the migration and invasion of ICC cells. Overexpression of HSPB8 and BAG3 in vivo promoted the lung metastasis ability of ICC cells. The HSPB8-BAG3 chaperone complex promotes ICC cell migration and invasion by regulating CASA-mediated degradation of Filamin A, offering insights for enhancing ICC therapeutic strategies.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2396694"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104700","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

Tripartite motif-containing protein 50 suppresses triple-negative breast cancer progression by regulating the epithelial-mesenchymal transition. 含三方基序蛋白 50 通过调节上皮-间充质转化抑制三阴性乳腺癌的进展。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-13 DOI: 10.1080/15384047.2024.2427410

Danxiang Chen, Jing Jiang, Wei Zhang, Xinlin Li, Qidong Ge, Xia Liu, Xujun Li

{"title":"Tripartite motif-containing protein 50 suppresses triple-negative breast cancer progression by regulating the epithelial-mesenchymal transition.","authors":"Danxiang Chen, Jing Jiang, Wei Zhang, Xinlin Li, Qidong Ge, Xia Liu, Xujun Li","doi":"10.1080/15384047.2024.2427410","DOIUrl":"10.1080/15384047.2024.2427410","url":null,"abstract":"Background and objectives: Tripartite motif-containing protein 50 (TRIM50) is a recently discovered E3 ubiquitin ligase that participates in tumor progression. TRIM50 is overexpressed in many cancers, although few studies focused on TRIM50's role in breast cancer.Methods: We overexpressed TRIM50 in triple-negative breast cancer cell lines using plasmid and found that TRIM50 upregulation markedly reduced breast cancer cell proliferation, clone formation, and migration, as well as promoted breast cancer cell apoptosis. Western blotting revealed that accumulated TRIM50 resulted in both mRNA and protein depletion of SNAI1, and partially attenuated the epithelial-mesenchymal transition (EMT) induced by SNAI1.Results: In this study, we demonstrate that TRIM50 is downregulated in human breast cancer and that its overexpression closely correlates with diminished invasion capacity in breast cancer, suggesting that TRIM50 may serve as a diagnostic marker and therapeutic target.Conclusion: TRIM50 plays a key role in breast cancer proliferation and potentially serves as a prognostic and therapeutic target.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2427410"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615190","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

The critical role of tumor microbiome in cancer immunotherapy. 肿瘤微生物组在癌症免疫疗法中的关键作用。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-01-19 DOI: 10.1080/15384047.2024.2301801

Liu Yang, Qi Wang, Lijuan He, Xingyu Sun

引用次数: 0

Neuroendocrine gene subsets are uniquely dysregulated in prostate adenocarcinoma. 神经内分泌基因亚群在前列腺癌中出现独特的失调。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-06-26 DOI: 10.1080/15384047.2024.2364433

Nicole M Naranjo, Anne Kennedy, Anna Testa, Cecilia E Verrillo, Adrian D Altieri, Rhonda Kean, D Craig Hooper, Jindan Yu, Jonathan Zhao, Oliver Abinader, Maxwell W Pickles, Adam Hawkins, William K Kelly, Ramkrishna Mitra, Lucia R Languino

{"title":"Neuroendocrine gene subsets are uniquely dysregulated in prostate adenocarcinoma.","authors":"Nicole M Naranjo, Anne Kennedy, Anna Testa, Cecilia E Verrillo, Adrian D Altieri, Rhonda Kean, D Craig Hooper, Jindan Yu, Jonathan Zhao, Oliver Abinader, Maxwell W Pickles, Adam Hawkins, William K Kelly, Ramkrishna Mitra, Lucia R Languino","doi":"10.1080/15384047.2024.2364433","DOIUrl":"10.1080/15384047.2024.2364433","url":null,"abstract":"Prostate cancer has heterogeneous growth patterns, and its prognosis is the poorest when it progresses to a neuroendocrine phenotype. Using bioinformatic analysis, we evaluated RNA expression of neuroendocrine genes in a panel of five different cancer types: prostate adenocarcinoma, breast cancer, kidney chromophobe, kidney renal clear cell carcinoma and kidney renal papillary cell carcinoma. Our results show that specific neuroendocrine genes are significantly dysregulated in these tumors, suggesting that they play an active role in cancer progression. Among others, synaptophysin (SYP), a conventional neuroendocrine marker, is upregulated in prostate adenocarcinoma (PRAD) and breast cancer (BRCA). Our analysis shows that SYP is enriched in small extracellular vesicles (sEVs) derived from plasma of PRAD patients, but it is absent in sEVs derived from plasma of healthy donors. Similarly, classical sEV markers are enriched in sEVs derived from plasma of prostate cancer patients, but weakly detectable in sEVs derived from plasma of healthy donors. Overall, our results pave the way to explore new strategies to diagnose these diseases based on the neuroendocrine gene expression in patient tumors or plasma sEVs.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2364433"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11212568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455466","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

BRG1 promotes liver cancer cell proliferation and metastasis by enhancing mitochondrial function and ATP5A1 synthesis through TOMM40. BRG1 通过 TOMM40 增强线粒体功能和 ATP5A1 合成，从而促进肝癌细胞增殖和转移。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-08 DOI: 10.1080/15384047.2024.2375440

Yongfeng Hui, Junzhi Leng, Dong Jin, Genwang Wang, Kejun Liu, Yang Bu, Qi Wang

{"title":"BRG1 promotes liver cancer cell proliferation and metastasis by enhancing mitochondrial function and ATP5A1 synthesis through TOMM40.","authors":"Yongfeng Hui, Junzhi Leng, Dong Jin, Genwang Wang, Kejun Liu, Yang Bu, Qi Wang","doi":"10.1080/15384047.2024.2375440","DOIUrl":"10.1080/15384047.2024.2375440","url":null,"abstract":"Hepatocellular carcinoma (HCC) is one of the most lethal malignant tumors worldwide. Brahma-related gene 1 (BRG1), as a catalytic ATPase, is a major regulator of gene expression and is known to mutate and overexpress in HCC. The purpose of this study was to investigate the mechanism of action of BRG1 in HCC cells. In our study, BRG1 was silenced or overexpressed in human HCC cell lines. Transwell and wound healing assays were used to analyze cell invasiveness and migration. Mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) detection were used to evaluate mitochondrial function in HCC cells. Colony formation and cell apoptosis assays were used to evaluate the effect of BRG1/TOMM40/ATP5A1 on HCC cell proliferation and apoptosis/death. Immunocytochemistry (ICC), immunofluorescence (IF) staining and western blot analysis were used to determine the effect of BRG1 on TOMM40, ATP5A1 pathway in HCC cells. As a result, knockdown of BRG1 significantly inhibited cell proliferation and invasion, promoted apoptosis in HCC cells, whereas BRG1 overexpression reversed the above effects. Overexpression of BRG1 can up-regulate MMP level, inhibit mPTP opening and activate TOMM40, ATP5A1 expression. Our results suggest that BRG1, as an oncogene, promotes HCC progression by regulating TOMM40 affecting mitochondrial function and ATP5A1 synthesis. Targeting BRG1 may represent a new and effective way to prevent HCC development.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2375440"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11236295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558159","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

NAALADL2-AS2 functions as a competing endogenous RNA to regulate apoptosis and drug resistance in DLBCL. NAALADL2-AS2作为一种竞争性内源性RNA调节DLBCL的细胞凋亡和耐药性。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-22 DOI: 10.1080/15384047.2024.2432690

Xiaoli Xu, Juan Liu, Cheng Fang, Xu Deng, Danxia Zhu, Jingting Jiang, Changping Wu

{"title":"NAALADL2-AS2 functions as a competing endogenous RNA to regulate apoptosis and drug resistance in DLBCL.","authors":"Xiaoli Xu, Juan Liu, Cheng Fang, Xu Deng, Danxia Zhu, Jingting Jiang, Changping Wu","doi":"10.1080/15384047.2024.2432690","DOIUrl":"10.1080/15384047.2024.2432690","url":null,"abstract":"To explore role of NAALADL2-AS2 as ceRNA in DLBCL. Fluorescence in situ hybridization was used to determine location of NAALADL2-AS2 in cells and to verify its expression in DLBCL tissues. The miRNAs interacting with NAALADL2-AS2 and related regulatory genes were identified by small interfering RNA (siRNA) assay, luciferase reporter assay, fluorescent quantitative polymerase chain reaction, western blotting. DLBCL cells transfected with NAALADL2-AS2 siRNA or control siRNA were treated with doxorubicin, rituximab at different concentrations alone or in combination. The growth curves, drug sensitivity changes of cells before and after transfection were detected by MTT assay, ATP-TCA drug sensitivity test. Cell proliferation was detected by BrdU cell proliferation assay, and apoptosis was detected by Annexin V-fluorescein isothiocyanate/propidium iodide staining. The effects and mechanisms of NAALADL2-AS2 on proliferation, apoptosis, drug resistance of DLBCL cells were studied at cellular level. We confirmed expression of NAALADL2-AS2 in both cytoplasm and nuclei of DLBCL cells. Additionally, we observed elevated levels of NAALADL2-AS2 in DLBCL tissues. We discovered that NAALADL2-AS2 functions as ceRNA to inhibit expression of miR-34a, miR-125a, whereas overexpression of NAALADL2-AS2 indirectly upregulates expression of BCL-2. Interfering with NAALADL2-AS2 promoted apoptosis in DLBCL cells, resulting in approximately a 40% increase in sensitivity to doxorubicin and rituximab. In vivo experiments further confirmed that targeting NAALADL2-AS2 effectively suppressed tumor growth, leading to upregulation of miR-34a and miR-125a, downregulation of BCL-2, and enhanced apoptosis in DLBCL cells, which significantly improved their sensitivity to doxorubicin and rituximab by approximately 50%. These results indicate that NAALADL2-AS2/miR-34a, miR-125a/BCL-2 networks hold promise as therapeutic targets for treatment of DLBCL.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2432690"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686228","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