Identification of HDAC4 as a target of gamma-catenin that regulates the oncogenic K-Ras-mediated malignant phenotype of Rat2 cellsopen access
- Authors
- Yim, Ji-Hye; Baek, Jeong-Hwa; Lee, Chang-Woo; Kim, Mm-Jung; Yun, Hong Shik; Hong, Eun-Hee; Lee, Su-Jae; Park, Jong Kuk; Um, Hong-Duck; Hwang, Sang-Gu
- Issue Date
- Jul-2013
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- gamma-Catenin; HDAC4; Lef1; Oncogenic K-Ras; Rat2 fibroblast cells
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.436, no.3, pp.436 - 442
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 436
- Number
- 3
- Start Page
- 436
- End Page
- 442
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/26692
- DOI
- 10.1016/j.bbrc.2013.05.122
- ISSN
- 0006-291X
- Abstract
- The mechanisms by which activated Ras accelerates malignant transformation of normal cells are not fully understood. Here, we characterized the role and molecular mechanism of gamma-catenin in regulating the malignant phenotype of Rat2 cells induced by codon 12-mutant K-Ras (K-Ras12V). Suppression of gamma-catenin signaling by K-Ras12V was an early event and played a crucial role in promoting the acquisition of a highly metastatic phenotype of Rat2 cells. Notably, the gene encoding histone deacetylase 4 (HDAC4) was identified as a target of gamma-catenin during this process. The transcription factor, lymphoid enhancer-binding factor-1 (Lef1), was involved in the modulation of HDAC4 transcription, and disruption of this pathway was a key event in promoting the invasion and migration of K-Ras12V-transduced Rat2 cells. Thus, our findings extend the range of targets for the development of new drugs for the therapy of oncogenic K-Ras-driven cancer. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
- Files in This Item
-
- Appears in
Collections - 서울 자연과학대학 > 서울 생명과학과 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.