The overexpression of miR-218-5p in cervical cancer (CC) cell lines decreases migration, invasion and proliferation. The objective was to identify target genes of miR-218-5p and the signaling pathways and cellular processes that they regulate. The relationship between the expression of miR-218-5p and RUNX2 and overall survival in CC as well as the effect of the exogenous overexpression of miR-218-5p on the level of RUNX2 were analyzed. The target gene prediction of miR-218-5p was performed in TargetScan, miRTarBase and miRDB. Predicted target genes were subjected to gene ontology (GO) and pathway enrichment analysis using the Kyoto Encyclopaedia of Genes and Genomes (KEGG). The miR-218-5p mimetic was transfected into C-33A and CaSki cells, and the miR-218-5p and RUNX2 levels were determined by RT–qPCR. Of the 118 predicted targets for miR-218-5p, 86 are involved in protein binding, and 10, including RUNX2, are involved in the upregulation of proliferation. Low miR-218-5p expression and a high level of RUNX2 are related to poor prognosis in CC. miR-218-5p overexpression is related to decreased RUNX2 expression in C-33A and CaSki cells. miR-218-5p may regulate RUNX2, and both molecules may be prognostic markers in CC.

Persistent infection with Helicobacter pylori (H. pylori) is an important factor in gastric diseases. The vacA and cagA virulence factors of H. pylori contribute to the development of these diseases. Triple therapy containing clarithromycin has been used to eradicate this infection. Unfortunately, resistance to this antibiotic is the primary cause of treatment failure. This study aimed to determine the prevalence of clarithromycin resistance-associated mutations and to assess the relationship between virulence factors and Mexican patients infected with H. pylori. The cagA and vacA genotypes were determined by multiplex PCR. Furthermore, a qPCR was used to identify mutations of the 23S rRNA gene. This study reported a prevalence of 84.3% of H. pylori among patients with gastric diseases, and the vacA s1m1/cagA+ genotype was the most frequent (44.8%) in antrum and corpus. Analysis of the 23S rRNA gene revealed a 19.8% prevalence of clarithromycin resistance-associated mutations. The most prevalent mutations were A2143G (56%) and A2142C (25%). A significant association (p < 0.05) between the A2142G and the vacA s1m1/cagA+ genotype was detected. In conclusion, we report a high prevalence (>15%) of clarithromycin resistance-associated mutations, and we found an association between the genotypes of virulence factors and a mutation in the 23S rRNA gene.

Background: Cervical cancer (CC) ranks as the third most common cancer in incidence and mortality in females worldwide. Let-7c is a tumor suppressor miRNA, and its role has been little studied in CC. Runt-related transcription factor 1 (RUNX1) is upregulated in several human cancers, such as colorectal cancer. It is a transcription factor that promotes cell proliferation, metastasis, chemotherapy resistance and angiogenesis in colorectal cancer. In this study, we performed a bioinformatic analysis to understand how Let-7c and RUNX1 are involved in the development of CC. Methods: We performed a bioinformatic analysis of Let-7c in CC using GSE and TCGA datasets from GEO, KM-plotter, miRPathDB and Enrich databases. Then, we conducted a comprehensive analysis of RUNX1’s role in CC using TCGA, GSE and HPA datasets from OncoDB, CISTROME, ExPASy, Alibaba, ALGGEN, ENCODE, IGV, GEO, KM-plotter and DiseaseMeth databases. Results: We found that Let-7c expression is decreased in CC. Interestingly, we identified a transcription factor known as RUNX1, as a potential target of Let-7c. Finally, we suggest that RUNX1 could regulate the expression of several genes, promoting CC. Conclusions: The Let-7c/RUNX1 axis promotes CC.