OBJECTIVETo investigate the signaling pathways involved in β-arrestin1-induced proliferation of K562 cells.

METHODSWe established stable cell lines K562-siβ1 and K562-β1 by lentivirus-mediated β-arrestin1 knock-down or overexpression in K562 cells, with cells transfected with non-specific siRNA as the control (K562-Ctrl). The proliferation of these cells were evaluated by cell counting and CCK-8 assays. Western blotting was used to detect the expression of JNK and p-JNK in the cells, and co-immunoprecipitation (Co-IP) assay was employed to investigate the interaction between β-arrestin1 and Src.

RESULTSK562-β1 cells showed significantly greater but K562-siβ1 cells had significantly lower proliferation ability and cell survival rate than K562-Ctrl cells. Western blotting showed that β-arrestin1 specifically enhanced the expression of p-JNK, and the JNK inhibitor SP600125 obviously suppressed p-JNK and cell proliferation of K562 cells. Co-IP assay revealed the binding of β-arrestin1 to Src.

CONCLUSIONSIn K562 cells, β-arrestin1 activates JNK signaling pathway by binding to Src to promote the cell proliferation.

Arrestins ; metabolism ; Cell Proliferation ; Cell Survival ; Humans ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; metabolism ; MAP Kinase Signaling System ; RNA, Small Interfering ; beta-Arrestins