ALG3 drives UCEC progression via MYC-dependent fatty acid metabolism

Background Uterine corpus endometrial carcinoma (UCEC) is one of the most common tumors in the female reproductive system, which is an important cause of death in women. ALG3 is high expression in UCEC, but it’s molecular mechanism is still unclear. Methods The ALG3 expression in UCEC was analyzed by TCGA-UCEC database. The cell proliferation was detected with CCK-8, EdU and colony formation assays. Cells apoptosis was analyzed by flow cytometry. Wound healing and transwell assays were performed to detect cell migration. The protein levels were analyzed via western blot. The intracellular triglycerides and cholesterol were analyzed by microplate reader. Xenograft mouse models were used to explore the effect of ALG3 on UCEC in vivo . Results ALG3 was highly expressed in UCEC. Patients with high ALG3 expression have poor prognosis. Additionally, the silence of ALG3 inhibited the proliferation and migration of UCEC cells, while promoted apoptosis. However, overexpression of ALG3 produced opposite results. ALG3 knockdown suppressed the MYC level and fatty acid metabolism in UCEC cells. Subsequently, the fatty acid metabolism, cell proliferation, cell migration and cell anti-apoptosis were promoted with MYC overexpressed in UCEC cells. In vivo , the ALG3 knockdown suppressed the progression of UCEC and fatty acid metabolism. Conclusion ALG3 enhanced MYC-mediated fatty acid metabolism to promote UCEC growth and metastasis, and inhibit cell apoptosis. ALG3 could be used as a new therapeutic target for UCEC.