// Tongtong Wang 2, * , Jing Du 3, * , Bingyu Chen 1 , Wei Zhang 4 , Zhen Wang 1 , Ke Hao 1 , Xin Wang 2 , Yi Zhou 2 , Qiaojuan Zhu 2 , Xiangmin Tong 2 and Ying Wang 1, 2 1 Department of Blood Transfusion, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, China 2 Clinical Research Institute, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, China 3 Department of Laboratory Medicine, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, China 4 Department of Hepatopancreatobiliary Surgery, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, China * These authors contributed equally to this work Correspondence to: Ying Wang, email: nancywangying@163.com Xiangmin Tong, email: tongxiangmin11@163.com Keywords: Xiao-Ai-Ping; chronic myeloid leukemia; proliferation; apoptosis; β-catenin Received: August 08, 2017 Accepted: November 16, 2017 Published: January 04, 2018 ABSTRACT The active ingredients of Xiao-Ai-Ping (XAP) injection are Marsdeniae tenacissimae extraction, which is a traditional Chinese herb has been used to treat multiple diseases for a long time. However, the possible roles and mechanisms of XAP in chronic myeloid leukemia (CML) still remain unknown. In this study, we examined the effects of XAP on proliferation and apoptosis of K562 cells (CML cell line) and peripheral blood mononuclear cell (PBMCs) from CML patients. Here, we found that XAP could inhibit the proliferation of K562 cells and induce the apoptosis of K562 cells via mitochondrial pathway. In addition, XAP inhibited the migration of K562 cells through downregulating the expression levels of chemokine SDF-1 and its receptor CXCR-4. In addition, XAP down-regulated β-catenin and CyclinD1 level, and up-regulated GSK3β level in K562 cells. Interestingly, over-expression of β-catenin restored the XAP-induced apoptosis of K562 cells. Furthermore, XAP significantly inhibited the proliferation and induced the apoptosis of PBMCs from CML patients, compared with healthy people. In conclusion, XAP could inhibit the proliferation and migration of CML cells, and induce the apoptosis of CML cells through down-regulation of β-catenin and SDF1/CXCR-4 signaling.