New insights of RA-V cyclopeptide as an autophagy inhibitor in human COLO 320DM cancer cell lines

Abstract

Colon cancer is the leading cause for the malignancy in the gastrointestinal tract. Autophagy is a self-degradation process of the unnecessary, injured and aged organelles and proteins in the cell, which is followed by recovering of degraded products. Apoptosis is a programmed cell death which is characterized by membrane blebbing, chromosome condensation and nuclear fragmentation. Apoptosis and autophagy can occur frequently in a cell, predominantly in a series preceding apoptosis through autophagy by the formation of autophagosomes. In current research, the impact of autophagy inhibition and apoptosis activation were found to be the targeted strategies to treat colon cancer. This study is focused on the apoptotic potential of RA-V, a natural cyclopeptide through the inhibition of protective autophagy in colon cancer cells. Growth inhibitory properties were observed in the RA-V treated (125 μM) colo 320DM cells using cell viability assay. RA-V induced apoptosis of colo 320DM cells at the maximum concentration of 125 μM, which was observed using DAPI and Annexin - PI staining methods. In this study we also examined the mechanistic role of RA-V (125 μM) in and colo 320DM cells in the presence of Rapamycin (mTOR inhibitor) and chloroquine (autophagy inhibitor) using MDC and AO staining methods.