Human MMP-2(Matrix Metalloproteinase 2) ELISA Kit

Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) has been demonstrated to be oncogenic. The aim of the present study was to examine the effects of SNHG12 on the progression of endometrial cancer (EC). The expression levels of SNHG12 and microRNA (miR)-4429 were assessed in EC cell lines by reverse transcription-quantitative PCR. Plasmids, including SNHG12 short hairpin RNAs (shRNAs), shRNA negative control (NC), SNHG12 overexpression (OV), OV-NC, miR-4429 mimic and mimic-NC, were transfected into RL95-2 cells. Post-transfection, Cell Counting Kit-8, Transwell Matrigel and wound-healing assays were performed to assess cell proliferation, invasion and migration, respectively. Cell cycle phase distribution was assessed by flow cytometry. The protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 were detected by western blotting. miR-4429 target genes were predicted by bioinformatics analysis using target prediction online tools; the findings of this analysis were verified using a dual-luciferase reporter system. Identified as a target of miR-4429, SNHG12 was overexpressed in EC cell lines with decreased expression of miR-4429. Further experiments demonstrated that SNHG12 silencing and overexpression of miR-4429 markedly suppressed proliferation, migration and invasion of RL95-2 cells, arrested cells in the G(1) phase, and markedly downregulated the expression of MMP2 and MMP9. The opposite effects were observed in miR-4429 mimic-transfected RL95-2 cells after SNHG12 was overexpressed. The findings of the present study established the role of SNHG12 and miR-4429 in EC. Therefore, targeting the SNHG12/miR-4429 axis could serve as a potential future therapeutic target for treatment of EC.

Esophageal squamous cell carcinoma (ESCC) is a common cancer in China and has a high mortality rate. MicroRNAs (miRs) are a family of post-transcriptional regulators, which negatively regulate target gene expression. miR-613 has been revealed to be a diagnostic and prognostic biomarker in ESCC. However, the role of miR-613 in ESCC remains unclear. In the present study, miR-613 expression was identified to be reduced in tumor tissues in comparison with corresponding adjacent normal tissues. TargetScan and a dual-luciferase reporter assay verified glucose-6-phosphate dehydrogenase (G6PD) as a direct target of miR-613. In contrast with miR-613, G6PD expression was increased in tumor tissues compared with matched healthy tissues. Furthermore, overexpression of miR-613 inhibited cell migration and invasion of Eca109 cells compared with controls, while G6PD overexpression reversed the inhibition induced by miR-613, as determined by wound healing and Transwell assays. In addition, miR-613 overexpression decreased the mRNA and protein expression of G6PD, matrix metalloproteinase (MMP)2 and MMP9, and reduced the phosphorylation of signal transducer and activator of transcription 3 (STAT3) compared with controls, while G6PD reversed the effects of miR-613. However, miR-613 and G6PD did not affect the expression of STAT3. In conclusion, the aforementioned results suggest that miR-613 targets G6PD to suppress ESCC cell migration and invasion through reduced MMP2 and MMP9 expression and inactivation of the STAT3 signaling pathway. Thus, the present study may provide a new molecular foundation for treatment of ESCC.