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Low‐expression of E‐cadherin in leukaemia cells causes loss of homophilic adhesion and promotes cell growth
Author(s) -
Rao Qing,
Wang JiYing,
Meng Jihong,
Tang Kejing,
Wang Yanzhong,
Wang Min,
Xing Haiyan,
Tian Zheng,
Wang Jianxiang
Publication year - 2011
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100456
Subject(s) - cadherin , stromal cell , microbiology and biotechnology , cell adhesion molecule , cell adhesion , haematopoiesis , bone marrow , chemistry , adhesion , gene silencing , cell , biology , cancer research , stem cell , immunology , biochemistry , organic chemistry , gene
E‐cadherin (epithelial cadherin) belongs to the calcium‐dependent adhesion molecule superfamily and is implicated in the interactions of haematopoietic progenitors and bone marrow stromal cells. Adhesion capacity to bone marrow stroma was impaired for leukaemia cells, suggesting that a breakdown of adhesive mechanisms governed by an adhesion molecule may exist in leukaemic microenvironment. We previously found that E‐cadherin was low expressed in primary acute leukaemia cells compared with normal bone marrow mononuclear cells. In this study, we investigate the functional importance of low E‐cadherin expression in leukaemia cell behaviours and investigate its effects in the abnormal interaction of leukaemic cells with stromal cells. After expression of E‐cadherin was restored by a demethylating agent in leukaemia cells, E‐cadherin‐specific adhesion was enhanced. Additionally, siRNA (small interfering RNA)‐mediated silencing of E‐cadherin in Raji cells resulted in a reduction of cell homophilic adhesion and enhancement of cell proliferation and colony formation. These results suggest that low expression of E‐cadherin contributes to the vigorous growth and transforming ability of leukaemic cells.