Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2011.12.099
Title: RAS oncogenic signal upregulates EZH2 in pancreatic cancer
Authors: Fujii, S.
Fukamachi, K.
Tsuda, H.
Ito, K.
Ito, Y. 
Ochiai, A.
Keywords: EZH2
Pancreatic cancer
RAS
RUNX3
Issue Date: 20-Jan-2012
Citation: Fujii, S., Fukamachi, K., Tsuda, H., Ito, K., Ito, Y., Ochiai, A. (2012-01-20). RAS oncogenic signal upregulates EZH2 in pancreatic cancer. Biochemical and Biophysical Research Communications 417 (3) : 1074-1079. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2011.12.099
Abstract: The neoplastic transformation by mutant RAS is thought to require remodeling of expression of an entire set of genes. However, the underlying mechanism for initiation of gene expression remodeling in tumorigenesis remains elusive. This study was aimed to define the oncogenic role of EZH2, a histone modifier protein that is induced by oncogenic mutant RAS, using pancreatic cancers of transgenic rats exogenously expressing human mutant RAS. Immunohistochemical observation of preneoplastic or cancerous lesions in the animal model suggested that upregulation of Ezh2 protein is an initiating event in pancreatic carcinogenesis. MEK-inhibition or Elk-1-knockdown downregulated EZH2, and MEK-inhibition or EZH2-knockdown restored expression of a tumor suppressor, RUNX3 in human and rat pancreatic cancer cells activated by the oncogenic RAS. Furthermore, Elk-1- or EZH2-knockdown inhibited growth of the cancer cells. These results strongly suggested that the oncogenic RAS upregulates EZH2 through MEK-ERK signaling, resulted in downregulation of tumor suppressors including RUNX3 in pancreatic carcinogenesis. © 2011 Elsevier Inc.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/125443
ISSN: 0006291X
DOI: 10.1016/j.bbrc.2011.12.099
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