In this study, we planned to investigate the function and potential mechanisms of Alpha‐1,3‐mannosyltransferase (ALG3) in oral squamous cell carcinoma (OSCC). Data from TCGA were used to analyze ALG3 expression and its effect on the prognosis of patients with OSCC. KEGG enrichment analysis was applied to explore the pathways related to ALG3. ALG3 expression was measured by qPCR and Western blot. Cell counting kit‐8, colony formation, and transwell assays were implemented to detect the effects of ALG3 on malignant biological properties of OSCC cells. The expression of key proteins related to CDK‐Cyclin pathway was detected by Western blot. The expression of ALG3 in OSCC samples was higher than that of the control samples, and the increase of ALG3 expression was related to unfavorable prognosis of OSCC patients. Additionally, the elevated expression of ALG3 was associated with pathological stage, lymph node metastasis, and primary lesion in OSCC patients. ALG3 depletion blocked the growth and movement of OSCC cells, while over‐expression ALG3 reversed these phenomena. Moreover, exhaustion of ALG3 resulted in decreased expression of MCM7/CCNB2/CDK1/PCNA, while these phenomena were inversed after ALG3 up‐regulation. The enhancement of ALG3 expression promoted the aggressive biological behaviors of OSCC cells probably by promoting CDK‐Cyclin pathway.

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Background: In this study, we planned to investigate the function and potential mechanisms of Alpha-1,3-mannosyltransferase (ALG3) in oral squamous cell carcinoma (OSCC). Methods: Data from The Cancer Genome Atlas (TCGA) was used to analyze ALG3 expression and its effect on the prognosis of patients with OSCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was applied to explore the signaling pathways related to ALG3. In OSCC cells, ALG3 expression was measured by qPCR and western blot. Cell counting kit-8, colony formation, and transwell assays were implemented to detect the effects of ALG3 on the malignant biological properties OSCC cells. The expression of key proteins related to CDK-Cyclin pathway was detected by western blot. Results: The expression of ALG3 in OSCC samples was higher than that of the control samples, and the increase of ALG3 expression was related to unfavorable prognosis of OSCC patients. Additionally, the elevated expression of ALG3 was associated with pathological stage, lymph node metastasis and primary lesion in OSCC patients. ALG3 depletion blocked the growth, colony formation, invasion and migration of OSCC cells, while over-expression ALG3 reversed these phenomena. Moreover, exhaustion of ALG3 resulted in decreased expression of MCM7, CCNB2, CDK1 and PCNA, while these phenomena were inversed after ALG3 up-regulation. Conclusions: The enhancement of ALG3 expression promoted the aggressive biological behaviors of OSCC cells probably by promoting CDK-Cyclin pathway.