Nitidine chloride (NC) exhibits
tumor suppressive function in a variety of human
cancers. However, the molecular mechanism of NC-triggered anti-
cancer activity has not been fully elucidated. In the present study, we aim to investigate the anti-
tumor molecular basis of NC in
prostate cancer cells. Multiple approaches including MTT, FACS, wound healing assay, Transwell invasion assay, Transfection, and Western blotting were performed. We found that NC inhibited cell growth and induced apoptosis in
prostate cancer cells. Moreover, NC suppressed cell migration and invasion in
prostate cancer cells. Notably, we found that NC decreased the expression of YAP
oncoprotein in
prostate cancer cells. Downregulation of YAP enhanced the anti-
tumor function mediated by NC in
prostate cancer cells. On the contrary, upregulation of YAP abrogated the anti-
cancer activity of NC treatment in
prostate cancer cells. Our findings indicate that NC could be useful as a YAP inhibitor for the treatment of
prostate cancer cells.