Deubiquitination of UTP14A stabilizes HIF-1α and promotes melanoma angiogenesis

Abstract

Abstract Objective To discuss the effects of UTP14A on the proliferation, migration and angiogenesis of melanoma, HIF-1α and its downstream pathway, and offer new clues for the diagnosis and treatment of melanoma. Methods After over expression/knockdown of UTP14A, the effects of UTP14A on proliferation, migration, invasion of melanoma cells and angiogenesis of HUVEC cells were observed by CCK8, plate cloning, transwell and angiogenesis assay. CoIP and immunofluorescence were used to identify the interaction between UTP14A and HIF-1α. The subcutaneous tumorigenesis was performed in nude mice. Tumor size and weight were observed, and angiogenesis mimicry of melanoma tissue was observed by HE staining. Results The results of CCK8 assay, plate cloning assay and mouse subcutaneous tumor formation assay showed that UTP14A promoted the proliferation of melanoma in vivo and in vitro. Transwell experiment demonstrated that UTP14A promotes melanoma migration and invasion. HE staining of mouse tumor tissue indicated that UTP14A promotes the angiogenesis. It was found that UTP14A could up-regulate the expression of HIF-1α. The response experiment verified that UTP14A upstream of HIF-1α. IP experiment confirmed that UTP14A stabilizes HIF-1α by deubiquitinating. Conclusion UTP14A promotes the progression of melanoma, and UTP14A promotes the proliferation, migration, invasion and angiogenesis of melanoma by stabilizing HIF-1α through deubiquitinating.