Open AccessDual action of apolipoprotein E‐interacting HCCR‐1 oncoprotein and its implication for breast cancer and obesity
Author(s) -
Ha SeonAh,
Shin Seung Min,
Kim Hyun Kee,
Kim Sanghee,
Namkoong Hong,
Lee Youn Soo,
Kim Hae Joo,
Jung Sang Min,
Lee Yu Sun,
Chung Yeun Jun,
Park Yong Gyu,
Jung Sang Seol,
Kim Jin Woo
Publication year - 2009
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2009.00652.x
Subject(s) - breast cancer , medicine , obesity , apolipoprotein e , oncogene , cancer research , cancer , endocrinology , apolipoprotein b , oncology , cholesterol , immunology , cell cycle , disease
Obese women have an increased risk for post‐menopausal breast cancer. The physiological mechanism by which obesity contributes to breast tumourigenesis is not understood. We previously showed that HCCR‐1 oncogene contributes to breast tumourigenesis as a negative regulator of p53 and detection of HCCR‐1 serological level was useful for the diagnosis of breast cancer . In this study, we found that the HCCR‐1 level is elevated in breast cancer tissues and cell lines compared to normal breast tissues. We identified apolipoprotein E (ApoE) interacting with HCCR‐1. Our data show that HCCR‐1 inhibits anti‐proliferative effect of ApoE, which was mediated by diminishing ApoE secretion of breast cancer cells. Finally, HCCR‐1 induced the severe obesity in transgenic mice. Those obese mice showed severe hyperlipidaemia. In conclusion, our results suggest that HCCR‐1 might play a role in the breast tumourigenesis while the overexpression of HCCR‐1 induces the obesity probably by inhibiting the cholesterol‐lowering effect of ApoE. Therefore, HCCR‐1 seems to provide the molecular link between the obesity and the breast cancer risk.