Rabbit Anti-Human MAPK1 / ERK2 (aa310-360) polyclonal antibody

Purpose: To explore the clinicopathological value and prospective function of microRNA-517a-3p (miR-517a- 3p) in bladder cancer (BC). Methods: The clinical importance of miR-517a-3p expression and genetic alteration in BC was unraveled by using The Cancer Genome Atlas (TCGA), cBioPortal, Gene Expression Omnibus (GEO) and ArrayExpress. The potential target genes of miR-517a-3p were obtained via the combination of predicted genes and down-regulated genes post miR-517a-3p transfection in vitro from microarray (GSE39093). The probable signaling pathways were further evaluated with multiple bioinformatics approaches. Results: MiR-517a-3p expression was significantly higher in the samples of pathologic N stage (N1-N3), pathologic stage (III-IV) and patients with lymphovascular invasion than that of their counterparts (P<0.05) based on data from TCGA. The amplification was the only alteration type which counted for 3% (14/412) in BC as indicated by cBioPortal. A total of 858 genes were gained by prediction from at least two predicting programs. Compared to control cells, there were 4844 genes down-expressed after BC cells (BOY and T24) were transfected with miR-517a-3p. Only "hsa05200: Pathways in cancer" was significantly enriched via Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis (P<0.05). Three significant pathways were discovered in PANTHER pathway analysis (P<0.05). Hub genes, such as CREB1, MAPK1, RPS6KA5, SMAD3 and PPARA, were identified by protein-protein interaction. Conclusion: The results in this study indicate that miR-517a-3p may play a potential role in the occurrence and development of BC, especially its genetic alteration, via various signal pathways. However, the exact mechanism still needs to be ascertained by in vitro and in vivo experiments.

Breast cancer is the most frequent cancer among women worldwide. Tumor immunology suggests relationships between the immune system, chronic inflammation, and cancer. The immune system may either prevent or promote carcinogenesis. Here, we evaluated molecular signaling pathways common in inflammation and cancer and detected the microRNAs which play pivotal roles in mediating these pathways. Using bioinformatics assays, signaling pathways common in inflammation and cancer, and microRNAs mediating these pathways were identified. MiR-590 was selected and cloned into the pLenti-III-eGFP vector and transfected into the breast cancer cell lines. The expression level of microRNA and the candidate genes was evaluated by real-time quantitative reverse transcription polymerase chain reaction, and the apoptosis level in transfected cells was measured by Annexin V-7AAD assay. The cell migration was tested by real-time quantitative reverse transcription polymerase chain reaction for MMP2/MMP9. The expression levels of miR-590 and the selected genes (i.e. JAK2, PI3K, MAPK1, and CREB) were measured 72 h after transfection. While miR-590 showed an over-expression, the genes were significantly down-regulated. A significant increase was observed in apoptosis level in both cell lines and MMP2/MMP9 was significantly decreased in MDA-MB-231 cells. MiR-590 was selected as a microRNA which triggers and down-regulates critical genes of signaling pathways similar in cancer and inflammation. Following the miR-590 treatment, JAK2, PI3K, MAPK1, and CREB were down-regulated and the apoptosis level was increased in breast cancer cell lines. Apparently, some microRNAs can be good candidates for novel treatments of cancer. Although miR-590 showed good results in this study, further studies are required to investigate the role of miR-590 in breast cancer therapy.