Bufalin inhibits glycolysis-induced cell growth and proliferation through the suppression of Integrin β2/FAK signaling pathway in ovarian cancer

American Journal of Cancer Research

Haoran Li¹  Yangyang Pang²  Shuang Hu³  Mengjiao Li⁴  Lihua Chen⁵  Fei Liu⁶ 

[1] Department of Gynecological Oncology and Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China;Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China;Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai 200032, China;Institute of Urology, Lanzhou University Second Hospital, Lanzhou University, Lanzhou 730000, China;Key Laboratory of Urological Diseases, Lanzhou University, Lanzhou 730000, China;School of Pharmacy, Anhui Medical University, Hefei 230031, China

关键词: Bufalin;    glucose metabolism;    ITGB2;    FAK;    ovarian cancer;   

DOI  :  

学科分类：肿瘤学

来源: e-Century Publishing Corporation

【 摘 要 】

Bufalin is the major digoxin-like component of the traditional Chinese medicine Chansu and has obvious anti-tumor effect in major malignancies, but the role of bufalin in glucose metabolism in ovarian cancer remains illustrated. Here, we sought to elucidate the regulatory function of bufalin on cell glucose metabolism in ovarian cancer. The treatment of bufalin on ovarian cancer cells effectively inhibited glucose uptake and lactate production in ovarian cancer cells. The expression levels of glycolysis-related proteins, including GLUT4, LDHB and HK2, were decreased by the treatment of bufalin detected by qRT-PCR and immunoblotting. Mechanistically, bufalin exerted its anti-tumor effect by targeting ITGB2/FAK signaling pathway in vitro and in vivo, which could be rescued by the introduction of ITGB2 cDNA in ovarian cancer cells. These findings provide evidence that bufalin inhibited cellular glycolysis-induced cell growth and proliferation through repression of the ITGB2/FAK pathway, indicating that bufalin may be developed as a chemotherapeutic agent to treat ovarian cancer.

【 授权许可】

CC BY-NC