烯醇化酶ENO1抑制非小细胞肺癌细胞上皮间质转换

BACKGROUND AND OBJECTIVE: It has been proven that epithelial-mesenchymal transition (EMT) is a critical process which is precisely regulated by multiple signaling pathways during the progression and metastasis of non-small cell lung cancer (NSCLC). Canonical MAPK signaling is essential to transforming growth factor β (TGFβ)-induced EMT. Using the NSCLC cell line A549 as a model, the aim of this study is to explore the molecular mechanism of ENO1 affecting EMT. METHODS: We established an A549 strain stably overexpressing ENO1. Cell mobility was measured by the wound-healing assay. EMT-related molecular alterations were detected by Western blot analysis. The effect of ENO1 on EMT was also detected by TGFβ-1-inducing assay. EGF-stimulating assay was performed to illustrate ERK1/2 phosphorylation changes resulting from ENO1 overexpression. RESULTS: Overexpressed ENO1 inhibited the mobility of A549 (P < 0.05), as well as the expression of the mesenchymal markers N-cadherin and vimentin, but upregulated the epithelial marker E-cadherin. TGFβ-inducing assay also showed that the negative effect of ENO1 on EMT. ERK1/2 phosphorylation was also obviously suppressed by ENO1 in the EGF-stimulating assay. CONCLUSION: In NSCLC cells, ENO1 overexpression can inhibit EMT in vitro by suppressing ERK1/2 phosphorylation.