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- Title
HCCRBP-1 directly interacting with HCCR-1 induces tumorigenesis through P53 stabilization.
- Authors
Ha, Seon-Ah; Shin, Seung Min; Lee, Yong Jin; Kim, Sanghee; Kim, Hyun Kee; Namkoong, Hong; Lee, Heejeong; Lee, Youn Soo; Cho, Young-Seok; Park, Yong Gyu; Jeon, Hae Myung; Oh, Changkyu; Kim, Jin Woo
- Abstract
Oncogene HCCR-1 functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. HCCR transgenic mice developed breast cancers but it is unknown how HCCR-1 contributes to human tumorigenesis. This study identified a HCCR-1-binding protein 1 ( HCCRBP-1) as an HCCR binding partner by performing yeast two hybrid screening. Their endogenous interaction was further confirmed by coimmunoprecipitation experiments. These two proteins colocalized in the mitochondria. HCCRBP-1 was overexpressed in various human tumors. In addition, HCCRBP-1 alone converted NIH/3T3 cells into tumor cells in combination with no other oncogenes. HCCRBP-1 induced tumorigenesis by markedly activating PKC activities but decreasing the pro-apoptotic PKCα and PKCδ isoform levels. We observed that p53 stabilization also occurred with functional impairment in HCCRBP-1-transfected 293 cells, as indicated by defective induction of p21, MDM2 and bax. Indeed, HCCRBP-1 decreased p21 promoter activity probably via p53 stabilization leading to the defective function. These results indicate that HCCRBP-1 oncogene induces p53 stabilization and thereby contributes to tumorigenesis. © 2007 Wiley-Liss, Inc.
- Publication
International Journal of Cancer, 2008, Vol 122, Issue 3, p501
- ISSN
0020-7136
- Publication type
Article
- DOI
10.1002/ijc.23146