Targeting HER-2 Signal Pathway in LNCaP Prostate Cancer Cells by Sodium Butyrate

Objective To investigate the mechanisms underlying the antitumor effect of histone deacetylase inhibitor sodium butyrate on LNCaP prostate cancer cells. Methods Proliferation of LNCaP cells exposed to sodium butyrate was detected by MTT assay. Cell apoptosis was assayed by hoechst 33342 nuclei staining as well as apoptosis marker protein leaved PARP expression. The expression of HER-2 as well as downstream key signaling molecules was assayed by western blotting after sodium butyrate exposure. Results Sodium butyrate killed LNCaP cells with an EC50 value of 5.6mmol/L within 48 hours as well as inducing cell apoptosis. Sodium butyrate could downregulate HER-2 expression through suppression of HER-2 gene transcription.Activation of downstream signaling molecules such as Akt and Erk were also suppressed. Conclusion Sodium butyrate exhibits significant antitumor effect against LNCaP cells through suppression of HER-2 signaling pathway.