Cancer Biology & Therapy最新文献_第3页

WYC-209 inhibited GC malignant progression by down-regulating WNT4 through RARα. WYC-209 通过 RARα 下调 WNT4，从而抑制 GC 的恶性发展。

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-01-04 DOI: 10.1080/15384047.2023.2299288

Zhenyuan Qian, Wenfa Lin, Xufan Cai, Jianzhang Wu, Kun Ke, Zaiyuan Ye, Fang Wu

{"title":"WYC-209 inhibited GC malignant progression by down-regulating WNT4 through RARα.","authors":"Zhenyuan Qian, Wenfa Lin, Xufan Cai, Jianzhang Wu, Kun Ke, Zaiyuan Ye, Fang Wu","doi":"10.1080/15384047.2023.2299288","DOIUrl":"10.1080/15384047.2023.2299288","url":null,"abstract":"Gastric cancer (GC) has been a major health burden all over the world but there are fewer promising chemotherapeutic drugs due to its multidrug resistance. It has been reported that WYC-209 suppresses the growth and metastasis of tumor-repopulating cells but the effect on GC was not explored. MTT, colony formation, and transwell assays were performed to examine the effects of WYC-209 on the proliferation, colony growth, and mobility of GC cells. Western blotting and qRT-PCR were used to detect the expression of proteins and mRNA. RNA-seq and enrichment analyses were conducted for the differentially expressed genes and enriched biological processes and pathways. The rescue experiments were carried out for further validation. Besides, we constructed xenograft model to confirm the effect of WYC-209 in vivo. The dual-luciferase reporter and Chromatin immunoprecipitation were implemented to confirm the underlying mechanism. WYC-209 exerted excellent anti-cancer effects both in vitro and in vivo. Based on RNA-seq and enrichment analyses, we found that Wnt family member 4 (WNT4) was significantly down-regulated. More importantly, WNT4 overexpression breached the inhibitory effect of WYC-209 on GC progression. Mechanically, WYC-209 significantly promoted the binding between retinoic acid receptor α (RARα) and WNT4 promoter. WYC-209 exerts anti-tumor effects in GC by down-regulating the expression of WNT4 via RARα.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2299288"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10773637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139097377","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

Epigenetic silencing ZSCAN23 promotes pancreatic cancer growth by activating Wnt signaling. 表观遗传沉默 ZSCAN23 通过激活 Wnt 信号促进胰腺癌生长

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-01-16 DOI: 10.1080/15384047.2024.2302924

Qian Du, Meiying Zhang, Aiai Gao, Tao He, Mingzhou Guo

引用次数: 0

M6A modification regulates tumor suppressor DIRAS1 expression in cervical cancer cells. M6A 修饰调节宫颈癌细胞中肿瘤抑制因子 DIRAS1 的表达。

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-19 DOI: 10.1080/15384047.2024.2306674

Yu-Yan Wang, Lian-Hua Ye, An-Qi Zhao, Wei-Ran Gao, Ning Dai, Yu Yin, Xin Zhang

{"title":"M6A modification regulates tumor suppressor DIRAS1 expression in cervical cancer cells.","authors":"Yu-Yan Wang, Lian-Hua Ye, An-Qi Zhao, Wei-Ran Gao, Ning Dai, Yu Yin, Xin Zhang","doi":"10.1080/15384047.2024.2306674","DOIUrl":"10.1080/15384047.2024.2306674","url":null,"abstract":"DIRAS family GTPase 1 (DIRAS1) has been reported as a potential tumor suppressor in other human cancer. However, its expression pattern and role in cervical cancer remain unknown. Knockdown of DIRAS1 significantly promoted the proliferation, growth, migration, and invasion of C33A and SiHa cells cultured in vitro. Overexpression of DIRAS1 significantly inhibited the viability and motility of C33A and SiHa cells. Compared with normal cervical tissues, DIRAS1 mRNA levels were significantly lower in cervical cancer tissues. DIRAS1 protein expression was also significantly reduced in cervical cancer tissues compared with para-cancerous tissues. In addition, DIRAS1 expression level in tumor tissues was significantly negatively correlated with the pathological grades of cervical cancer patients. DNA methylation inhibitor (5-Azacytidine) and histone deacetylation inhibitor (SAHA) resulted in a significant increase in DIRAS1 mRNA levels in C33A and SiHa cells, but did not affect DIRAS1 protein levels. FTO inhibitor (FB23-2) significantly down-regulated intracellular DIRAS1 mRNA levels, but significantly up-regulated DIRAS1 protein levels. Moreover, the down-regulation of METTL3 and METTL14 expression significantly inhibited DIRAS1 protein expression, whereas the down-regulation of FTO and ALKBH5 expression significantly increased DIRAS1 protein expression. In conclusion, DIRAS1 exerts a significant anti-oncogenic function and its expression is significantly downregulated in cervical cancer cells. The m6A modification may be a key mechanism to regulate DIRAS1 mRNA stability and protein translation efficiency in cervical cancer.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2306674"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10878024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139899398","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

Association between the IL1B-511 C>T polymorphism and the risk of hematologic malignancies: data from a meta-analysis. IL1B-511 C>T 多态性与血液系统恶性肿瘤风险之间的关系：一项荟萃分析的数据。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-22 DOI: 10.1080/15384047.2024.2382503

Fabíola Silva Alves-Hanna, Felipe Rodolfo Pereira Silva, Daniele Sá Pereira, Alessandro Luiz Araújo Bentes Leal, Fábio Magalhães-Gama, Allyson Guimarães Costa

{"title":"Association between the IL1B-511 C>T polymorphism and the risk of hematologic malignancies: data from a meta-analysis.","authors":"Fabíola Silva Alves-Hanna, Felipe Rodolfo Pereira Silva, Daniele Sá Pereira, Alessandro Luiz Araújo Bentes Leal, Fábio Magalhães-Gama, Allyson Guimarães Costa","doi":"10.1080/15384047.2024.2382503","DOIUrl":"10.1080/15384047.2024.2382503","url":null,"abstract":"The relationship between the IL1B-511C>T (rs16944) polymorphism and the risk of developing hematologic malignancies remains controversial. Thus, we performed a meta-analysis to evaluate the association between IL1B-511C>T polymorphism and the risk of developing hematologic malignancies. A comprehensive search was conducted to identify all eligible studies on IL1B-511C>T polymorphism and hematologic malignancies. Twelve case-control studies, with 2,896 cases and 3,716 controls, were selected for the analysis. The overall data failed to indicate a significant association between IL1B-511C>T polymorphism and the risk of hematologic malignancies (OR:1.06, 95% Confidence Interval [CI]: 0.93-1.22). Moreover, non-significant associations were observed in a stratified analysis according to neoplasm type (multiple myeloma, Hodgkin's lymphoma, and non-Hodgkin's lymphoma), ethnicity (European and Asian), and Hardy-Weinberg equilibrium. In summary, our results suggest that there is no association between the IL1B-511C>T polymorphism and the risk of hematologic malignancies. As such, further large-scale studies are needed to confirm our findings.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2382503"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11268255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747530","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

Mechanism investigation of Forsythoside A against esophageal squamous cell carcinoma in vitro and in vivo. 连翘苷 A 对食管鳞状细胞癌的体内外作用机制研究

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-24 DOI: 10.1080/15384047.2024.2380023

Yingying Yang, Junru Shen, Peiyuan Deng, Ping Chen

{"title":"Mechanism investigation of Forsythoside A against esophageal squamous cell carcinoma in vitro and in vivo.","authors":"Yingying Yang, Junru Shen, Peiyuan Deng, Ping Chen","doi":"10.1080/15384047.2024.2380023","DOIUrl":"10.1080/15384047.2024.2380023","url":null,"abstract":"Context: Forsythoside A (FSA) was extracted from Forsythia suspensa, a traditional Chinese medicine, which has been demonstrated to exert anti-inflammatory, antibacterial, and other pharmacological effects. However, the anticancer effect of FSA in esophageal squamous cell carcinoma (ESCC) has not been documented.Objective: The present study aimed to elucidate the mechanism of FSA against ESCC.Materials and methods: Network pharmacology and molecular docking were employed to predict the mechanism. FSA was utilized to treat ESCC cell lines KYSE450 and KYSE30, followed by CCK-8 assay, cell cloning formation assay, flow cytometry, Western blot, RNA-seq analysis, and subsequent in vivo experiments.Results: Network pharmacology and molecular docking predicted that the therapeutic effect of FSA in ESCC is mediated through proteins such as BCL2 and BAX, influencing KEGG pathways associated with apoptosis. In vitro experiments showed that FSA inhibited cell proliferation and plate clone formation, promoted cell apoptosis and impacted the cell cycle distribution of G2/M phase by regulating BCL2, BAX, and p21. Further RNA-seq in KYSE450 cells showed that FSA regulated the expression of 223 genes, specifically affecting the biological process of epidermal development. In vivo experiments showed that gastric administration of FSA resulted in notable reductions in both tumor volume and weight by regulating BCL2, BAX, and p21. 16S rRNA sequencing showed that FSA led to significant changes of beta diversity. Abundance of 11 specific bacterial taxa were considerably changed following administration of FSA.Conclusions: This study presents a novel candidate drug against ESCC and establishes a foundation for future clinical application.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2380023"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11271126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751184","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

Exploring the molecular mechanisms and therapeutic potential of SMAD4 in colorectal cancer. 探索 SMAD4 在结直肠癌中的分子机制和治疗潜力。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-20 DOI: 10.1080/15384047.2024.2392341

Hui Shan, Guangyu Tian, Yeqing Zhang, Zhiyuan Qiu

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