Abstract
Vacuolar protein sorting-associated protein 16 homolog (VPS16) is a central member of the VPS core complex (VPS-C) and is reported to function as a tether protein involved in membrane fusion. However, a biological role for VPS16 in tumors remains largely unknown. Herein, we demonstrated that VPS16 was overexpressed in colorectal cancer (CRC) as revealed by qRT-PCR, western blotting, and immunohistochemical analyses. Elevated expression of VPS16 was positively correlated with tumor size and TNM stage, and Kaplan-Meier analysis showed an association between VPS16 and survival in CRC patients. Downregulation of endogenous VPS16 significantly suppressed CRC cell viability both in vitro and vivo; and while our mechanistic analysis showed that VPS16 depletion induced autophagy, but the autophagic flow was deficient as reflected by the inhibition of autolysosomal maturation. Overexpression of VPS16 also mediated oxaliplatin (OX) resistance by promoting the maturation of autolysosomes in CRC. VPS16 may therefore promote cell survival and thus serve as a useful target for cancer therapy in CRC.