Deregulated microRNAs (miRs) and their roles in carcinogenesis have attracted great attention in recent years. Although miR-204 was reportedly dysregulated in various types of cancer, its function and mechanism in cervical cancer remain unknown. The present study focused on the expression and mechanisms of miR-204 in cervical cancer development. Expression of miR-204 in cervical cancer tissues and non-tumor tissues was measured using PCR analysis. The effect of ectopic expression of miR-204 on cell motility was evaluated using wound-healing and Transwell invasion assays. Luciferase activity and western blot assays were used to verify the regulatory effect of miR-204 on its target gene. It was demonstrated that miR-204 was significantly decreased in primary cervical cancer tissues, and that downregulated miR-204 was associated with lymph node metastasis and poor survival. In addition, it was revealed that ectopic expression of miR-204 significantly inhibited the migratory and invasive ability of cervical cancer cells in vitro. In addition, bioinformatic prediction and experimental validation demonstrated that transcription factor 12 (TCF12) was a direct target of miR-204. Overexpression of TCF12 attenuated the inhibitory effect of miR-204 on cell motility. Taken together, the present data indicated that miR-204 is a metastasis-associated gene and may contribute to the progression of cervical cancer by regulating TCF12, providing novel insights, including that miR-204/TCF12 may be an important mechanism for cervical cancer metastasis.

Beckground:The association of MGMT (O6-methyguanine deoxyribonucleic acid methyltransferase) promoter hypermethylation with gastric cancer (GC) risk has been studied extensively, but the results remained unclear. Here, we performed a meta-analysis to evaluate whether promoter hypermethylation of the MGMT gene contributed to gastric pathogenesis.Methods:Relevant studies were identified by retrieving the PubMed, Web of Science, Embase, and China National Knowledge Infrastructure (CNKI) databases. The Newcastle–Ottawa Scale was applied to assess methodological quality of the included studies. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to evaluate the association of MGMT promoter hypermethylation with gastric pathogenesis. Moreover, STATA 12.0 software was used to summarize the extracted data in this meta-analysis.Results:Seventeen studies, comprising 1736 cases and 1291 controls, were included in this meta-analysis. The frequency of MGMT promoter hypermethylation in the GC group (32.97%) was significantly higher than those in the control group (18.00%) (OR = 2.83, CI = 1.93–4.15, P < .05). When stratified by cancer subtype, the results indicated that the frequency of MGMT promoter hypermethylation was significantly higher in gastric adenocarcinoma than in control group (OR = 3.47, CI = 1.06–11.35, P < .05). In addition, MGMT promoter hypermethylation significantly promoted distant metastasis and lymph node (LN) metastasis of gastric tumor (for distant metastasis, OR = 4.22, CI = 2.42–7.37, P < .05; for LN metastasis, OR = 1.56, CI = 1.14–2.13, P < .05). A significant association between MGMT promoter hypermethylation and TNM-stage was also found in the present meta-analysis (OR = 2.70, CI = 1.79–4.08, P < .05).Conclusion:The results of this meta-analysis suggested that MGMT gene-promoter hypermethylation was significantly associated with an increased risk of GC, especially in Asians. Furthermore, MGMT gene-promoter hypermethylation might be correlated with the distant metastasis and LN metastasis of GC.