SSX2IP promotes cell proliferation and migration in breast cancer by regulating FANCI.

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Xianfu Liu, Xiaojing Zhang, Yansong Chen, Jingwei Tang, Hao Zhang, Gongsheng Jin
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引用次数: 0

Abstract

Synovial sarcoma X breakpoint 2 interacting protein (SSX2IP) is expressed in various normal tissues and participates in the progression of human cancers. Nevertheless, the specific functions and underlying molecular mechanisms of SSX2IP in cancer, particularly in breast cancer, remain poorly understood. In this study, we aimed to explore the functional role of SSX2IP in breast cancer. Immunohistochemical staining, quantitative real-time PCR, and western blotting blot analysis were used to assess genes expression levels. By manipulating SSX2IP expression levels and conducting functional assays including Celigo cell counting assay or CCKCCK-8-8 assay, flow cytometry, wound healing assay, and Transwell assay, we explored the impact of SSX2IP on the malignant phenotype of breast cancer cells. Additionally, the in vivo tumor-suppressive ability of SSX2IP was investigated by tumor xenograft experiment. Our results revealed an upregulation of SSX2IP in the breast cancer. Functional assays demonstrated that SSX2IP knockdown inhibited cell proliferation and migration, induced apoptosis in vitro, as well as suppressed the tumor growth in vivo. Conversely, SSX2IP overexpression contributed to the malignant phenotype of breast cancer cells. Co-expression analysis showed that FA Complementation Group I (FANCI) was co-expressed with SSX2IP. Additionally, SSX2IP positively regulated FANCI expression and its interaction was verified by Co-IP.Co-IP. Furthermore, FANCI overexpression partially reversed the effects of SSX2IP knockdown on cell proliferation and metastasis. In summary, our findings revealed that SSX2IP contributes to the progression of breast cancer by regulating FANCI, hinting at its potential as a novel biomarker and therapeutic target for the treatment of breast cancer.

SSX2IP 通过调节 FANCI 促进乳腺癌细胞的增殖和迁移。
滑膜肉瘤 X 断点 2 互作蛋白(SSX2IP)在多种正常组织中表达,并参与人类癌症的进展。然而,人们对 SSX2IP 在癌症(尤其是乳腺癌)中的具体功能和潜在分子机制仍知之甚少。本研究旨在探讨 SSX2IP 在乳腺癌中的功能作用。研究采用免疫组化染色、实时定量 PCR 和 Western blotting 印迹分析来评估基因表达水平。通过调节 SSX2IP 的表达水平,并进行 Celigo 细胞计数试验或 CCKCCK-8-8 试验、流式细胞术、伤口愈合试验和 Transwell 试验等功能试验,我们探讨了 SSX2IP 对乳腺癌细胞恶性表型的影响。此外,我们还通过肿瘤异种移植实验研究了 SSX2IP 的体内抑瘤能力。结果显示,SSX2IP 在乳腺癌中上调。功能实验表明,体外敲除 SSX2IP 可抑制细胞增殖和迁移,诱导细胞凋亡,并抑制体内肿瘤的生长。相反,SSX2IP 过表达则会导致乳腺癌细胞的恶性表型。共表达分析表明,FA补体第一组(FANCI)与SSX2IP共表达。此外,SSX2IP 能正向调控 FANCI 的表达,其相互作用已通过 Co-IP.Co-IP 得到验证。此外,FANCI 的过表达部分逆转了 SSX2IP 敲除对细胞增殖和转移的影响。总之,我们的研究结果表明,SSX2IP通过调控FANCI促进了乳腺癌的进展,这预示着SSX2IP有可能成为治疗乳腺癌的新型生物标记物和治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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