PUS7 promotes the progression of pancreatic cancer by interacting ANLN to activate MYC pathway.

To investigate the role of pseudouridine synthase 7 (PUS7) in pancreatic cancer (PC) and explore its underlying molecular mechanisms. PUS7 role in the malignant biological function of PC cells was investigated by colony formation, EdU, flow cytometry, and transwell assays. PUS7 function on glycolysis of PC cells was determined through assessing the extracellular acidification rate and oxygen consumption rate. Besides, the potential molecular mechanism by which PUS7 affects PC was investigated via utilizing immunohistochemistry staining, western blot, qRT-PCR, and co-immunoprecipitation. Xenograft tumors were constructed using BALB/c nude mice. PUS7 was highly expressed in PC tissues. PUS7 significantly accelerated proliferation, mobility and glycolysis, but suppressed apoptosis in PC. Furthermore, PUS7 promoted the malignant biological function of PC cells by interacting anillin (ANLN). We also demonstrated that PUS7 promoted the malignant biological function of PC cells by activating the MYC pathway. PUS7 promoted PC progression via activating the MYC pathway in vivo. Our results indicated that PUS7 could promote cell proliferation, mobility and glycolysis, and inhibit apoptosis by interacting ANLN to activate the MYC pathway in PC.