PURPOSE: Previous studies have shown that MEX3C is an oncogene; however, its role in osteosarcoma (OS) development has not been reported. We aimed at investigating whether MEX3C could be engaged in the malignant progression of OS through regulating FGF14. METHODS: MEX3C levels in tumor tissues and adjacent ones of 52 OS patients were studied by quantitative real-time polymerase chain reaction (qRT-PCR), and the relationship between MEX3C expression and clinicopathological characteristics of OS patients was analyzed. At the same time, qRT-PCR further verified the MEX3C level in OS cell lines, and HOS and MG63 OS cell lines were selected to construct MEX3C overexpression and knockdown cell model, respectively. The impact of MEX3C on OS cell functions were determined by cell wound healing and transwell assay. In addition, the interaction between MEX3C and FGF14 was further determined by luciferase assay, western blot and recovery experiments. RESULTS: MEX3C had increased expression both in OS tissue samples and in OS cell lines. High expression of MEX3C was predictive of high incidence of nodal involvement or distant metastasis. Silencing MEX3C remarkably attenuated the migration ability of OS cells, while, conversely, overexpression enhanced that. Bioinformatics analysis and luciferase assay confirmed that MEX3C bind to FGF14 directly, and the expression of FGF14 was significantly reduced in OS tumor tissue specimens, and was negatively correlated with MEX3C. Overexpression of FGF14 was able to reverse the promoting effect of MEX3C on the crawling ability and invasiveness of OS cells. CONCLUSIONS: MEX3C was remarkably increased in OS tissues and was remarkably correlated with the incidence of metastasis of OS patients. In addition, MEX3C accelerated the malignant progression of OS through negatively modulating FGF14.
PURPOSE: Previous studies have shown that MEX3C is an oncogene; however, its role in osteosarcoma (OS) development has not been reported. We aimed at investigating whether MEX3C could be engaged in the malignant progression of OS through regulating FGF14. METHODS:MEX3C levels in tumor tissues and adjacent ones of 52 OS patients were studied by quantitative real-time polymerase chain reaction (qRT-PCR), and the relationship between MEX3C expression and clinicopathological characteristics of OS patients was analyzed. At the same time, qRT-PCR further verified the MEX3C level in OS cell lines, and HOS and MG63 OS cell lines were selected to construct MEX3C overexpression and knockdown cell model, respectively. The impact of MEX3C on OS cell functions were determined by cell wound healing and transwell assay. In addition, the interaction between MEX3C and FGF14 was further determined by luciferase assay, western blot and recovery experiments. RESULTS:MEX3C had increased expression both in OS tissue samples and in OS cell lines. High expression of MEX3C was predictive of high incidence of nodal involvement or distant metastasis. Silencing MEX3C remarkably attenuated the migration ability of OS cells, while, conversely, overexpression enhanced that. Bioinformatics analysis and luciferase assay confirmed that MEX3C bind to FGF14 directly, and the expression of FGF14 was significantly reduced in OS tumor tissue specimens, and was negatively correlated with MEX3C. Overexpression of FGF14 was able to reverse the promoting effect of MEX3C on the crawling ability and invasiveness of OS cells. CONCLUSIONS:MEX3C was remarkably increased in OS tissues and was remarkably correlated with the incidence of metastasis of OS patients. In addition, MEX3C accelerated the malignant progression of OS through negatively modulating FGF14.