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

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/ß-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/ß-catenin signaling, providing a promising biomarker and treatment approach for preventing PCa.

Role of miR-490-3p in blocking bladder cancer growth through targeting the RNA-binding protein PCBP2.

MiR-490-3p is regarded as a tumor suppressor in many cancers, but whether miR-490-3p is involved in the development of bladder cancer remains unknown. BALB/c nude mice (male, 15-20 g) were used to investigate the role of MiR-490-3p in bladder cancer. The relationship between miR-490-3p and PCBP2 involved in bladder cancer regulation were determined. Cell viability, proliferation, and cell cycle were estimated by cell counting kit-8 (CCK-8) assay, 5-bromo-2'-deoxyuridine (BrdU) detection, and flow cytometry analysis, respectively. In animal experiments, lentivirus was transfected into bladder cancer cells to overexpress miR-490-3p, which were then injected into mice and the change of tumor volume was assessed. Principal findings: The expression of MiR-490-3p was decreased in bladder cancer cells. Overexpression of miR-490-3p inhibited bladder cancer cell viability and proliferation. Moreover, overexpression of miR-490-3p caused cell cycle arrest in bladder cancer cells. The inhibitory effect of miR-490-3p on bladder cancer cells growth could be counteracted by enhancing PCBP2 expression. In vivo, bladder cancer growth in mice was blocked by miR-490-3p upregulation. MiR-490-3p suppressed bladder cancer growth and bladder cancer cell proliferation by down-regulating PCBP2 expression.