NCAPH promotes proliferation as well as motility of breast cancer cells by activating the PI3K/AKT pathway.

Abstract

This study aimed to assess the expression of NCAPH in human breast cancer, and to investigate its effects on breast cancer cells. Bioinformation analysis was performed to analyze the expression of NCAPH in human breast cancer tissues and normal tissues in TCGA database. qPCR and Immunoblot assays were performed to clarify the expression of NCAPH in breast cancer tissues and cell lines, respectively. CCK-8, colony formation, FCM, transwell, and immunoblot assays were performed to reveal the effects of NCAPH on breast cancer proliferation, cell cycle, motility and EMT of breast cancer cells. Additionally, immunoblot assays were performed to investigate the effects of NCAPH on the PI3K/AKT pathway in breast cancer. We found that NCAPH was highly expressed in human breast cancer cell lines. The depletion of NCAPH suppressed the viability of breast cancer cells. Further, we noticed that its downregulation restrained breast cancer cell migration as well as invasion, and the EMT process. Mechanically, we noticed that NCAPH mediated the PI3K/AKT pathway, and therefore contributed to breast cancer progression. In summary, NCAPH has the potential to serve as a breast cancer target.