[AKR1B10 promotes proliferation of breast cancer cells by activating Wnt/β-catenin pathway].

Objective To investigate the effect of aldosterone reductase family 1 member B10 (AKR1B10) on breast cancer cell proliferation and its mechanism. Methods AKR1B10 was overexpressed in MCF-7 cells and knocked down in BT-20 cells to establish both AKR1B10 overexpression and knockdown cell lines. The effect of AKR1B10 overexpression and knockdown on breast cancer cell proliferation was examined by CCK-8 assay. Real-time quantitative PCR was performed to detect AKR1B10 mRNA levels in breast cancer tissues and paired normal tissues. Western blot analysis was used to determine the protein levels of AKR1B10, beta-catenin, cyclin D1, survivin, c-myc in breast cancer tissues and AKR1B10 overexpression/knockdown breast cancer cell lines. Results The expression of AKR1B10 was higher in breast cancer tissues. With AKR1B10 overexpression in MCF-7 cells, cell proliferation was promoted, and the expression levels of beta-catenin, cyclin D1, c-myc and survivin were elevated. Meanwhile, knockdown of AKR1B10 in BT-20 breast cancer cells reduced cell proliferation and the expression levels of beta-catenin, cyclin D1, c-myc and survivin. Conclusion AKR1B10 is highly expressed in breast cancer and promotes breast cancer cell proliferation by activating Wnt/beta-catenin signaling pathway.