AP3M2: A key regulator from the nervous system modulates autophagy in colorectal cancer

Abstract

Colorectal cancer (CRC) affects approximately a million people annually with a mortality rate of 50 %, accounting for 8 % of cancer-related deaths globally. Molecular characterization by The Cancer Genome Atlas could be useful in these tumor subtypes to reveal "druggable" genes. Our study focuses on the significance of the AP3M2 gene (adaptor-related protein complex 3 subunit mu 2) as a potential oncogene by employing RNA interference to inactivate AP3M2. AP3M2, inplicated in protein trafficking to lysosomes pathway and specialized organelles in neuronal cells, was amplified in CRC cell lines. The Knockdown of AP3M2 significantly reduced the viability of three CRC cell lines HCT-116, CACO2, and HT29. Intriguingly, our findings revealed an interaction between AP3M2 expression and autophagy-related genes, as well as reactive oxygen species (ROS) levels in CRC cell lines. These results suggest that targeting AP3M2 could provide a powerful strategy for CRC treatment through autophagy-ROS mechanism.