• J Exp Clin Canc Res · Sep 2016

    Inhibition of YAP suppresses CML cell proliferation and enhances efficacy of imatinib in vitro and in vivo.

    • Hui Li, Zhenglan Huang, Miao Gao, Ningshu Huang, Zhenhong Luo, Huawei Shen, Xin Wang, Teng Wang, Jing Hu, and Wenli Feng.
    • Department of Clinical Hematology, Key Laboratory of Laboratory Medical Diagnostics Designated by the Ministry of Education, Chongqing Medical University, No.1, Yixueyuan Road, Chongqing, 400016, China.
    • J Exp Clin Canc Res. 2016 Sep 6; 35 (1): 134.

    BackgroundYes-associated protein (YAP), an essential component of Hippo pathway, was identified as an oncoprotein which participated in the progression of various malignancies. However, its role in chronic myeloid leukemia (CML) remains to be further clarified.MethodsThe expression of YAP in CML cells was determined by western blotting. Next, the effects of YAP knockdown and YAP inhibitor on CML cells were evaluated by MTT assay, flow cytometry (FCM) and Wright's staining. Moreover, K562 induced mice model was employed to further investigate the role of YAP in vivo.ResultsYAP was overexpressed in CML cells. Knockdown of YAP by si-RNA or inhibition the function of YAP using verteporfin (VP) not only inhibited the proliferation, induced the apoptosis of CML cells but also reduced the expression of YAP target genes c-myc and survivin. Additionally, VP enhanced the efficacy of imatinib (IM) in vitro and suppressed leukemogenesis in vivo.ConclusionOur results indicate that YAP may play an important role in the proliferation and leukemogenesis of CML cells. Genetic or pharmacological inhibition of YAP provides a novel treatment strategy for CML.

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