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Abstract 714: Cannabidiol-induced apoptosis is mediated by activation of Noxa in human colorectal cancer cells

Authors :
Bo Ram Kim
Yoon A. Jeong
Hye Kyeong Yun
Seong Hye Park
Yoo Jin Na
Jung Lim Kim
Bu Gyeom Kim
Dae Young Kim
Dae Hee Lee
Min Jee Jo
Soyeon Jeong
Sang Cheul Oh
Source :
Cancer Research. 79:714-714
Publication Year :
2019
Publisher :
American Association for Cancer Research (AACR), 2019.

Abstract

Cannabidiol (CBD), one of the compounds present in the marijuana plant, has anti-tumor properties, but its mechanism is not well known. The authors aimed to evaluate the apoptotic action of CBD in colorectal cancer cells (CRC), and focused on its effects on the novel pro-apoptotic Noxa-reactive oxygen species (ROS) signaling pathway. CBD experiments were performed using the colorectal cancer cell lines HCT116 and DLD-1. CBD induced an apoptosis by regulating many pro- and anti-apoptotic proteins, of which Noxa showed a significantly higher expression. To understand the relationship between Noxa and CBD-induced apoptosis, authors downregulated Noxa levels using siRNA and confirmed that the expression of apoptosis markers was decreased. After ROS production was blocked, the level of Noxa also decreased, suggesting that ROS is involved in the regulation of Noxa. The Noxa and ROS are well-known pro-apoptotic signaling agents. As a result, CBD was found to induce apoptosis in a Noxa-and-ROS-dependent manner. The effects of CBD treatment were re-demonstrated in vivo, thus confirming its role as a novel, reliable anticancer drug Citation Format: Hye Kyeong Yun, Soyeon Jeong, Yoon A Jeong, Min Jee Jo, Jung lim Kim, Seong Hye Park, Bo Ram Kim, Yoo Jin Na, Dae Young Kim, Bu Gyeom Kim, Dae Hee Lee, Sang Cheul Oh. Cannabidiol-induced apoptosis is mediated by activation of Noxa in human colorectal cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 714.

Details

ISSN :
15387445 and 00085472
Volume :
79
Database :
OpenAIRE
Journal :
Cancer Research
Accession number :
edsair.doi...........fd32b589078f308c3813efaae38e169a