Curcumin selectively induces colon cancer cell apoptosis and S cell cycle arrest by regulates Rb/E2F/p53 pathway

Abstract

ObjectiveCurcumin is a natural active product extracted from turmeric, has been reported to have anticancer properties against various tumors. However, the effect of curcumin on colon cancer remains still unclear. Our aimed to investigate the anti-colon cancer properties of curcumin in vitro, and determine the molecular mechanisms underlying these effects. MethodsViability assays including CCK8 and LDH were used to measure cell proliferation. Flow cytometry was performed to detect cell apoptosis and cell cycle distribution. qRT-PCR and Western blotting was used for measuring genes/protein expression/activation in apoptotic and pro-carcinogenic cellular signaling pathways. Finally, the results were confirmed using a xenograft tumor model that comprised of mice. ResultsIn vitro, Our data showed that curcumin preferentially and, in a dose, dependent way inhibited colon cancer cells proliferation, but was not toxic to normal colon mucosa epithelial cells. Curcumin induced apoptosis through a p53-mediated mechanism, pro-apoptotic proteins Bax was upregulated, and cell cycle arrest at S phase by inhibited the expression of cell cycle related proteins, phosphorylation of Rb signaling pathway proteins and E2F family transcription factors. Finally, the mouse xenograft model confirmed the suppressive effect of curcumin on tumor growth in vivo. ConclusionCurcumin may be a potential strategy for the treatment of colon cancer.