China Oncology ›› 2015, Vol. 25 ›› Issue (10): 780-784.doi: 10.3969/j.issn.1007-3969.2015.10.004

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Research on the cytostatic effect of bufalin on cervical carcinoma cells and the related mechanism

LIU Fei1, LI Haoran1, CHENG Xi1, LI Mengjiao1, WANG Ziliang2, YANG Li3   

  1. 1.Department of Gynecological Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China; 2. Department of Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China; 3.Department of Gynecological Oncology, Zhejiang Cancer Hospital, Hangzhou 310002, Zhejiang, China
  • Online:2015-10-30 Published:2015-12-17
  • Contact: CHENG Xi E-mail: cheng_xi1@hotmail.com

Abstract: Background and purpose: Cervical cancer remains the second leading cause of death in gynecologic malignancies partially because of resistance to chemotherapy. Bufalin, a component of the traditional Chinese medicine Chansu, has been widely used in cancer treatment in China. This study aimed to investigate the effects of bufalin on inhibiting the proliferation of ME180 and C33A and explore its possible mechanism. Methods: The cytostatic effects of bufalin on ME180 and C33A cells were evaluated by CCK8 assay (cell counting kit-8). Glucose levels in ME180 and C33A cells were measured using glucose assay kit. Then the alterations of GLUT1 (glucose transporter 1) and HK2 (hexokinase 2) gene expression were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expressions of proto-oncogene C-MYC and HIF1α (hypoxia-inducible factor 1α) were determined by Western blot. Results: According to the results of CCK-8, bufalin can significantly inhibit the proliferation of carcinoma cells ME180 and C33A (P=0.027, P=0.018). Test on glycometabolism indicated that glucose uptake in cells treated with bufalin decreased (P=0.034, P=0.036). Results from real-time PCR showed that the expression of glycometabolism related indicators GLUT1 (P=0.019) and HK2 (P=0.016) levels were significantly down-regulated in bufalin treated group. Western blot showed that the expression of C-MYC and HIF1αin cells with bufalin treatment was down-regulated markedly. Conclusion: Bufalin can inhibit the proliferation of the cervical carcinoma cells ME180 and C33A through inhibition of their glucose metabolism.

Key words: Bufalin, Cervical neoplasm, Cellular proliferation, Glucose metabolism