ArticleBMC oral health2025
Laminin-gamma2 promotes oral squamous cell carcinoma growth by activating the p-ERK/c-Myc signaling pathway.
Article in BMC oral health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOral squamous cell carcinoma (OSCC) is one of the most common types of head and neck carcinoma. As limited therapies for OSCC are available, the examination of new targets could expand therapeutic options. Recent studies have found the abnormal expression of Laminin-gamma2 (LAMC2) in OSCC. However, the mechanism by which LAMC2 participates in the occurrence and development of OSCC has not been fully clarified.
methodsBioinformatics analysis was used to Identification of hub genes in oral tumor tissues of OSCC. Overall survival probability and cumulative incidence of LAMC2 were explored in OSCC patients in the GSE41613 dataset. Cell proliferation assays, transwell assays were conducted to observe the change in OSCC proliferation ability and invasion. Gain or loss of function experiments were performed to observe the effect of LAMC2 on the signaling pathway. And we examined the mRNA and protein levels of LAMC2 in human OSCC tissue to explore the biological significance of LAMC2. Furthermore, Tumor formation assay was used to observe knocking down LAMC2 on tumorigenesis in OSCC cells in vivo.
resultsWe identified LAMC2, a crucial oncoprotein, were upregulated in human OSCC samples in TCGA datasets compared to healthy controls. The upregulated LAMC2 was related to poorer survival rates, increased the risk of OSCC-specific mortality, and there were significant differences in survival between the LAMC2 high and low expression groups. We also validated that the mRNA and protein expression of LAMC2 were upregulated in human OSCC samples compared with the para-tumor tissues. LAMC2 overexpression significantly enhanced cell proliferation and invasion. Mechanistically, overexpression of LAMC2 could increase the expression levels of p-ERK and c-Myc, while knockdown of LAMC2 resulted in the opposite effect. Moreover, the ERK inhibitor decreased ERK phosphorylation and reversed the OSCC phenotype induced by LAMC2 overexpression.
conclusionsLAMC2 enhances the cell proliferation, invasion of OSCC cells via the p-ERK/c-Myc axis, suggesting the crucial role of LAMC2 in the progression of OSCC and small molecule inhibitors targeting LAMC2 might be an effective treatment for OSCC patients.
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