SIRT6 Promotes the Progression of Prostate Cancer via Regulating the Wnt/ β -Catenin Signaling Pathway.

Autor: Zhang X; Department of Urology Surgery, The Wenzhou Central Hospital, The Dingli Clinical College of Wenzhou Medical University, Wenzhou, Zhejiang, China., Chen R; Department of Urology Surgery, The People's Hospital of Zhuji, Shao Xing, Zhejiang, China., Song LD; Department of Urology Surgery, The People's Hospital of Zhuji, Shao Xing, Zhejiang, China., Zhu LF; Department of Urology Surgery, The People's Hospital of Zhuji, Shao Xing, Zhejiang, China., Zhan JF; Department of Urology Surgery, The People's Hospital of Zhuji, Shao Xing, Zhejiang, China.
Jazyk: angličtina
Zdroj: Journal of oncology [J Oncol] 2022 Feb 25; Vol. 2022, pp. 2174758. Date of Electronic Publication: 2022 Feb 25 (Print Publication: 2022).
DOI: 10.1155/2022/2174758
Abstrakt: Sirtuin 6 (SIRT6), a DNA repair-related gene, has undergone an extremely thorough study for its involvement in the development of many different cancers. The objective of our study was to explore the function and mechanism of SIRT6-induced regulation of prostate cancer (PCa). RT-PCR was performed to validate the levels of SIRT6 in PCa cell lines. Cell proliferation, migration, and invasion of cells with SIRT6 knockdown were assessed using CCK-8 assay, colony formation assay, wound-healing assay, and transwell assay. Western blot was applied to assess the related proteins. We found that SIRT6 expression was distinctly upregulated in PCa specimens and cells. Loss-of-functional assays revealed that SIRT6 silence suppressed the proliferation and metastasis of PCa cells. Mechanistic studies revealed that SIRT6 silence inhibited Wnt/ β -catenin signaling and EMT progress. Overall, the study confirmed the upregulation of SIRT6 in patients with PCa and its association with the progression. SIRT6 promoted PCa progression by regulating Wnt/ β -catenin signaling, providing a promising biomarker and treatment approach for preventing PCa.
Competing Interests: The authors declare no conflicts of interest in this work.
(Copyright © 2022 Xian Zhang et al.)
Databáze: MEDLINE
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