ALG3 contributes to the malignancy of non-small cell lung cancer and is negatively regulated by MiR-98-5p.

Alpha-1,3-mannosyltransferase (ALG3) is an oncoprotein associated with multiple malignancies. We aimed to investigate the role and potential mechanisms of ALG3 in non-small cell lung cancer (NSCLC). We detected the expressions of ALG3 in NSCLC tissues and adjacent tissues by RT-PCR, western blot and immunohistochemistry, respectively. Chi-square test was used to analyze the correlation between ALG3 expression and pathological paremeters. Then we used shRNA to construct a low expression model of ALG3 in NCI-H292 and NCI-H460. CCK-8 assay and transwell assay were then performed to monitor the proliferation, migration and invasion of NSCLC cells. Western blot was to detect the expression of EMT-related indicators. Further, the interaction of miR-98-5p with ALG3 was verified by luciferase reporter assay. The expression of ALG3 in NSCLC tissues was higher than that in normal tissues, and the increase in ALG3 expression was significantly associated with higher T stage, lymph node metastasis, and poor tissue differentiation. Patients with high ALG3 expression had a worse prognosis. ALG3 knockdown inhibited the proliferation, migration and invasion of NSCLC cells. In addition, the knockdown of ALG3 resulted in increased expression of EMT-related protein E-cadherin, while N-cadherin and Vimentin expression was decreased. Dual luciferase assay confirmed that miR-98-5p can specifically bind to the 3'UTR of ALG3 and reduces its expression and activity. ALG3 can promote the progression of NSCLC and is negatively regulated by miR-98-5p.

Declaration of Competing Interest The authors declare that they have no Conflict of interest.