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HCCRBP‐3 induces tumorigenesis through direct interaction with HCCR‐1 in human cancers
Author(s) -
Ha Seon Ah,
Kim Hyun Kee,
Yoo Jin Ah,
Kim Sanghee,
Shin Seung Min,
Gong GiHwan,
Lee Yun Kyung,
Kim Jin Woo
Publication year - 2014
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.21945
Subject(s) - biology , carcinogenesis , cancer research , genetics , microbiology and biotechnology , computational biology , cancer
Human cervical cancer oncogene 1, HCCR‐1, is over‐expressed in various human tumors and appears to serve as a negative regulator of the p53 gene. HCCR‐1 transgenic mice developed breast cancers but it is unknown how HCCR‐1 contributes to tumorigenesis. We identified the HCCR‐1 binding protein 3 (HCCRBP‐3) as a binding partner for HCCR‐1. These two proteins co‐localized to the mitochondria. HCCRBP‐3 over‐expressed in various human tumors converted normal cells into tumor cells in vitro. Nude mice injected with NIH/3T3 cells stably transfected with HCCRBP‐3 also induced the tumor formation. In addition, p53 showed the functional impairment in HCCRBP‐3‐transfected cells as accompanied with defective induction of p21 and bax. In support of this, p21 promoter activities containing p53 responsive elements were inhibited by HCCRBP‐3 in a dose‐dependent manner. Therefore, our study suggests that HCCRBP‐3 contributes to the HCCR‐1 induced tumorigenesis by interrupting the p53 function. © 2013 Wiley Periodicals, Inc.