Abstract: Objective To investigate the signaling pathways involved in β-arrestin1-induced proliferation of K562 cells. Methods
We 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.
Results K562-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. Conclusions In K562 cells, β-arrestin1 activates JNK signaling pathway by binding to Src to promote the
cell proliferation.