Jump to main content
Jump to site search

Issue 44, 2015
Previous Article Next Article

α-Mangostin induces G1 cell cycle arrest in HCT116 cells through p38MAPK-p16INK4a pathway

Author affiliations

Abstract

α-Mangostin (α-MG), one of the active substances in Garcinia mangostana, has been shown to exhibit anti-cancer effects in various cancer cell types. α-MG treatment induces G1 arrest in cancer cell models through the induction of cyclin-dependent kinase inhibitors (CDKIs) and the subsequent loss of CDK activity. However, outside its role in the p53-p21CIP1 axis, the precise molecular mechanisms underlying the effect of α-MG on cell cycle arrest remain unclear. In this study, we observed that α-MG inhibits the proliferation of HCT116 cells in a dose-dependent manner. Interestingly, although the loss of p53 rescued the α-MG effect on cell cycle arrest, in agreement with previous reports, p21Cip1 expression was only marginally delayed in the absence of p53 after α-MG treatment. Instead, we found that the activation of p38 mitogen activated protein kinase (MAPK) and the subsequent downregulation of Bmi-1 also contributed to the induction of p16Ink4a, which is responsible for G1 arrest upon α-MG treatment. These findings indicate that α-MG exerts cytostatic effects on colon cancer cells by inducing G1 arrest via the p38MAPK-p16INK4a axis.

Graphical abstract: α-Mangostin induces G1 cell cycle arrest in HCT116 cells through p38MAPK-p16INK4a pathway

Back to tab navigation

Supplementary files

Article information


Submitted
14 Jan 2015
Accepted
09 Apr 2015
First published
09 Apr 2015

RSC Adv., 2015,5, 34752-34760
Article type
Paper
Author version available

α-Mangostin induces G1 cell cycle arrest in HCT116 cells through p38MAPK-p16INK4a pathway

S. Korm, H. Jeong, O. Kwon, J. Park, H. Cho, Y. Kim, Y. Chin and H. Cha, RSC Adv., 2015, 5, 34752
DOI: 10.1039/C5RA00780A

Social activity

Search articles by author

Spotlight

Advertisements