Abstract 4261: Upregulation of miR-34b, miR-892a and inhibition of p-glycoprotein play an important role for melatonin-induced apoptosis and autophagy in vincristine-resistant human oral cancer cells

Abstract

Abstract Multidrug-resistance was resistance of cells to a variety of drugs normally used in tumor treatment. The related mechanism of drug resistance in oral cancer has not been completely explained. Melatonin is an endogenously-produced molecule involved in active biological mechanisms including antiproliferation, oncogene expression modulation, antitumor invasion and migration, and anti-inflammatory, antioxidant, and antiangiogenic effects. Despite these numerous actions, the effect of melatonin on vincristine (VCR)-resistant human oral cancer cells still largely unknown. Present study analyzed the role of melatonin on VCR-resistant human oral cancer cells along with the underlying mechanism. We determined that melatonin induces apoptosis and autophagy of VCR-resistant oral cancer cell; these actions are mediated by AKT, p38, and JNK. Melatonin inhibits ABCB1 and ABCB4 expression in vitro/vivo. Melatonin decrease drug resistance and promotes VCR-resistant oral cancer cell execute apoptosis through upregulation of miR-892a and miR-34b-5p expression. The expression of miR-892a and miR-34b-5p are related with melatonin-induced apoptosis, but not autophagy. Thus, melatonin is a potential novel agent in chemotherapy for VCR-resistant human oral cancer cell lines. Citation Format: Shun-Fa Yang, Ming-Ju Hsieh, Chiao-Wen Lin. Upregulation of miR-34b, miR-892a and inhibition of p-glycoprotein play an important role for melatonin-induced apoptosis and autophagy in vincristine-resistant human oral cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4261.