DUXAP10 regulates proliferation and apoptosis of chronic myeloid leukemia via PTEN pathway

R. Yao, W.-T. Feng, L.-J. Xu, X.-M. Zhong, H. Liu, Y. Sun, L.-L. Zhou

Department of Oncology, The Affiliated Huai’an No. 1 People’s Hospital of Nanjing Medical University, Huai’an, China. bogy2004a@163.com

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• Hematology

OBJECTIVE: To investigate the role of DUXAP10 in chronic myelogenous leukemia (CML) and its underlying mechanism.

PATIENTS AND METHODS: We detected DUXAP10 expression in 82 CML patients, 12 normal controls, and CML cell line by qRT-PCR (quantitative real-time polymerase chain reaction). After transfection of si-DUXAP10 or si-PTEN in CML cell lines (K652, KG-1), we detected proliferation, cell cycle, and apoptosis by CCK-8 (cell counting kit-8), colony formation assay, and flow cytometry, respectively. Finally, protein expressions of p21, CDK2, Bcl-2, Bax, and PTEN were detected by Western blot.

RESULTS: DUXAP10 was upregulated in CML tissues and cells, which was gradually increased in the chronic phase (CP), acceleration phase (AP), and blast phase (BP) of CML. Knockdown of DUXAP10 in K652 and KG-1 cells can remarkably inhibit cell proliferation, promote cycle arrest and apoptosis. Western blot and flow cytometry results demonstrated that DUXAP10 can reduce apoptosis by inhibiting PTEN expression.

CONCLUSIONS: Overexpressed DUXAP10 accelerates the development and progression of CML by promoting cell proliferation, reducing cell cycle arrest and apoptosis via inhibiting PTEN expression.

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