Open AccessThe membrane molecule RCAS1 induces immune cell apoptosis via the RCAS1-RCAS1R pathway
Author(s) -
Yuanyuan Zhang,
Jie Zhu,
Hong Xiao,
Yunlian Zhou,
Keming Ren,
Xiaoli Shu,
Qingqing Wang
Publication year - 2013
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2013.1326
Subject(s) - jurkat cells , biology , apoptosis , hela , k562 cells , cancer cell , microbiology and biotechnology , transfection , immune system , cell cycle , cell culture , cancer research , cell , t cell , cancer , immunology , biochemistry , genetics
Tumor-associated antigen receptor-binding cancer antigen expressed on SiSo cells (RCAS1) has been identified as an estrogen-responsive gene and reportedly acts as a ligand for a putative receptor present in a variety of human cell lines and peripheral lymphocytes, thus leading them to apoptosis. In this study, we investigated the biological function of RCAS1 in vitro in inducing the apoptosis of immune cells. We detected the expression of the RCAS1 receptor (RCAS1R) in the cell lines, and investigated the mechanisms behind the apoptosis induced by RCAS1. HeLa cells were transfected with recombinant adenovirus Ad-RCAS1. RCAS1 induced the apoptosis of activated T cells, K562 cells and phytohemagglutinin (PHA)-activated Jurkat cells via the RCAS1-RCAS1R pathway. The expression of RCAS1R was induced. The intracellular overexpression of RCAS1 inhibited the growth of Jurkat and K562 cells. The expression of RCAS1 negatively correlated with the expression of glycogen synthase kinase 3β (GSK3β), but positively correlated with the expression of phosphorylated GSK3β (phGSK3β). RCAS1 expression was identified as a brown staining pattern in the breast cancer specimens. These findings may provide insight into the mechanisms through which tumor cells escape from immune surveillance.