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

Autor: Liu X; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China., Zhang X; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China., Chen Y; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China., Tang J; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China., Zhang H; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China., Jin G; Department of Surgical Oncology, the First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.
Jazyk: angličtina
Zdroj: Cell biology international [Cell Biol Int] 2024 Nov 12. Date of Electronic Publication: 2024 Nov 12.
DOI: 10.1002/cbin.12259
Abstrakt: 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.
(© 2024 International Federation for Cell Biology.)
Databáze: MEDLINE
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