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Journal of Cancer Prevention

Original Article

Journal of Cancer Prevention 2016; 21(1): 26-31

Published online March 30, 2016

https://doi.org/10.15430/JCP.2016.21.1.26

© Korean Society of Cancer Prevention

Dehydroglyasperin D Inhibits the Proliferation of HT-29 Human Colorectal Cancer Cells Through Direct Interaction With Phosphatidylinositol 3-kinase

Sung Keun Jung1,2, and Chul-Ho Jeong3

1Research Group of Nutraceuticals for Metabolic Syndrome, Korea Food Research Institute, Seongnam, Keimyung University, Daegu, Korea, 2Food Biotechnology Program, Korea University of Science and Technology, Daejeon, Keimyung University, Daegu, Korea, 3College of Pharmacy, Keimyung University, Daegu, Korea

Correspondence to :
Chul-Ho Jeong, College of Pharmacy, Keimyung University, 1095 Dalgubeol-daero, Dalseo-gu, Daegu 42601, Korea, Tel: +82-53-580-6638, Fax: +82-53-580-5164, E-mail: chjeong75@kmu.ac.kr, ORCID: Chul-Ho Jeong, http://orcid.org/0000-0003-4709-3497

Received: February 15, 2016; Revised: February 22, 2016; Accepted: February 22, 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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Background:

Despite recent advances in therapy, colorectal cancer still has a grim prognosis. Although licorice has been used in East Asian traditional medicine, the molecular properties of its constituents including dehydroglyasperin D (DHGA-D) remain unknown. We sought to evaluate the inhibitory effect of DHGA-D on colorectal cancer cell proliferation and identify the primary signaling molecule targeted by DHGA-D.

Methods:

We evaluated anchorage-dependent and -independent cell growth in HT-29 human colorectal adenocarcinoma cells. The target protein of DHGA-D was identified by Western blot analysis with a specific antibody, and direct interaction between DHGA-D and the target protein was confirmed by kinase and pull-down assays. Cell cycle analysis by flow cytometry and further Western blot analysis was performed to identify the signaling pathway involved.

Results:

DHGA-D significantly suppressed anchorage-dependent and -independent HT-29 colorectal cancer cell proliferation. DHGA-D directly suppressed phosphatidylinositol 3-kinase (PI3K) activity and subsequent Akt phosphorylation and bound to the p110 subunit of PI3K. DHGA-D also significantly induced G1 cell cycle arrest, together with the suppression of glycogen synthase kinase 3β and retinoblastoma phosphorylation and cyclin D1 expression.

Conclusions:

DHGA-D has potent anticancer activity and targets PI3K in human colorectal adenocarcinoma HT-29 cells. To our knowledge, this is the first report to detail the molecular basis of DHGA-D in suppressing colorectal cancer cell growth.

Keywords: PI3K, Dehydroglyasperin D, Colorectal neoplasms, Proliferation, Cell cycle

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