Depletion of VAX2 Restrains the Malignant Progression of Papillary Thyroid Carcinoma by Modulating ERK Signaling Pathway.

ABSTRACT

OBJECTIVE: Ventral anterior homeobox 2 (VAX2) gene is a key regulating factor for the development of the ventral region of the eye, and has recently attracted much attention from the cancer treatment field. Our study aimed to explore the effect of VAX2 on papillary thyroid carcinoma (PTC). METHODS: We determined the expression levels of VAX2 in PTC based on The Cancer Genome Atlas (TCGA) database. We then assessed the prognosis of patients with PTC, and analyzed the association between VAX2 expression and clinicopathological characteristics. Subsequently, we measured the biological functions of VAX2 in PTC using qRT-PCR, cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay, transwell assays and western blot. RESULTS: VAX2 was up-regulated in PTC tissues when compared with normal thyroid tissues, and high expression level of VAX2 was positively correlated with poor prognosis. Furthermore, knockdown of VAX2 significantly inhibited the proliferation, migration and invasion of PTC cells. Importantly, through western blot analysis, we found that the expression of phosphorylated-(p) ERK and p-MEK in ERK signaling pathway showed a significant decrease after knockdown of VAX2. CONCLUSION: These findings suggest that VAX2 may be involved in the malignant progression of PTC, and hold significant potential as a therapeutic target for PTC.