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

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.