VPS50 is required for the proliferation and survival of cervical cancer cells

Objective: Study of important molecules involved in the pathogene-sis of cervical cancer will be of great significance for the early screen -ing and treatment. Growing evidence suggests that Vacuolar protein sorting (VPS) proteins play roles in cancer biology. However, the role of VPS50 in cancers have not been explored. The purpose of this study is to explore the role of VPS50 in the progression of cervical cancer. Methods: In silico analysis was performed to explore the expression and mutation of VPS50 in several cancers. A shRNA against VPS50 were constructed to knockdown VPS50 in SiHa cells, which isa cervi-cal cancer cell line. Cell growth was detected by clone formation as-say and Celigo cell counting assay. Apoptosis rate was measured by flow cytometry and Caspase-3/7 Assay. PathScan intracellular signal -ing arrays kit was used to detect the changes of signaling molecules involved in Stress and Apoptosis pathway alter VPS50 knockdown in SiHa cells. Results: VPS50 is highly expressed in various cancers in-cluding cervical cancer, and various VPS50 mutations exist in can-cer cells. Down-regulation of VPS50 expression results in decreased cell proliferation and an inhibition of colony formation of SiHa cells. Moreover, VPS50 knockdown could significantly induce the apopto-sis of SiHa cells by activating the Stress and Apoptosis Pathway. Dis-cussion: Our study has demonstrated that VPS50 plays an essential role in the progression of cervical cancer and may serve as a potential therapeutic target for cervical cancer.