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Updated: Apr 11, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
[β-arrestin1 promotes chronic myeloid leukemia cell proliferation by activating JNK signaling pathway]
1Center for Clinical Molecular Medicine, Children's Hospital of Chongqing Medical University//Ministry of Education Key Laboratory of Child Development and Disorders//Key Laboratory of Pediatrics in Chongqing//Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing 400014, China.E-mail: stella8848@163.com.
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.
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