Jump to main content
Jump to site search


Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1 phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells

Abstract

Brosimone I is an isoprenoid-substituted flavonoid from Artocarpus heterophyllus. Here, we reported for the first time that brosimone I induced cell cycle G1 phase arrest and apoptosis in HCT116 human colon cancer cells. Brosimone I treatment increased cytosolic Ca2+ level, and subsequently activated the CaMKKβ-AMPK pathway. STO-609, a CaMKKβ inhibitor and compound C, an AMPK-specific inhibitor, attenuated brosimone I-induced loss of cell viability in HCT116 cells. Furthermore, brosimone I enhanced ER stress. Salubrinal, an ER stress inhibitor, reduced brosimone I-induced cell growth inhibition. In addition, brosimone I was found to increase ROS generation and the inhibition of ROS formation by NAC, a ROS inhibitor, attenuated brosimone I-induced cell death, cytosolic Ca2+ increase, and ER stress markers. Collectively, our findings reveal that brosimone I induces cell cycle G1 phase arrest and apoptosis via the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKKβ-AMPK signaling pathway.

Back to tab navigation

Supplementary files

Publication details

The article was received on 27 Nov 2018, accepted on 10 Apr 2019 and first published on 11 Apr 2019


Article type: Paper
DOI: 10.1039/C8FO02315H
Citation: Food Funct., 2019, Accepted Manuscript

  •   Request permissions

    Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1 phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells

    Y. Zhao, Y. Zhou and M. Wang, Food Funct., 2019, Accepted Manuscript , DOI: 10.1039/C8FO02315H

Search articles by author

Spotlight

Advertisements