β-arrestin1 promotes chronic myeloid leukemia cell proliferation by activating JNK signaling pathway
Abstract：Objective To investigate the signaling pathways involved inβ-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 thatβ-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 ofβ-arrestin1 to Src. Conclusions In K562 cells,β-arrestin1 activates JNK signaling pathway by binding to Src to promote the cell proliferation.
Keywords：β-arrestin1chronic myelocytic leukemiacell proliferationJNK
Publication Date：2015-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 677-681 )