Open AccessZNF251 promotes the progression of lung cancer by activating ERK signaling
Author(s) -
Zhong Chenxi,
Chen Chunji,
Yao Feng,
Fang Wentao
Publication year - 2020
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.14547
Subject(s) - lung cancer , kras , cancer research , mapk/erk pathway , regulator , downregulation and upregulation , biology , signal transduction , cancer , lung , medicine , microbiology and biotechnology , pathology , colorectal cancer , genetics , gene
Aberrant activation of ERK signaling is a hallmark of lung cancer. Although constitutively activating mutations of EGFR and KRAS contribute to the hyperactivation of ERK1/2, other mechanisms remain elusive. In this study, the zinc finger protein ZNF251 was found to be upregulated in clinical lung cancer samples, and it promoted the growth of lung cancer cells and the growth of primary lung KPC cells from mouse models (Ad‐Cre, Kras G12D , and P53 f/f ). In studying the molecular mechanism, ZNF251 was found to inhibit the expression of dual‐specificity phosphatase 6, a negative regulator of ERK activation, by directly binding to its promoter region. Taken together, our data indicate the tumor‐promoting effects of ZNF251 in lung cancer and suggest that ZNF251 is a therapeutic target.