Anti-ETS1 monoclonal antibody, clone 9B9

Increasing evidence indicates that numerous microRNAs (miRNAs) are altered in pancreatic ductal adenocarcinoma (PDAC), and their alterations significantly influence the malignant behaviour of PDAC. Therefore, identifying miRNAs associated with PDAC and their biological roles in the disease may provide promising therapeutic opportunities. Alteration of the expression of miRNA-766 (miR-766) has been previously reported in several types of human malignancy. However, to the best of our knowledge, whether miR-766 exhibits different expression patterns in PDAC and its underlying functions in the progression of PDAC remain to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect miR-766 expression levels in PDAC tissues and cell lines. The effects of miR-766 upregulation on PDAC cell proliferation and invasion were evaluated using MTT and invasion assays, respectively. The mechanisms underlying the role of miR-766 in PDAC cells were explored using bioinformatics analysis, luciferase reporter assay, RT-qPCR and western blot analysis. It was found that miR-766 was significantly downregulated in PDAC tissues and cell lines. The detailed roles of miR-766 in the progression of PDAC were characterised using Panc-1 and Aspc-1 cell lines. The results revealed that the upregulation of miR-766 restricted the proliferation and invasion of PDAC cells. Through a series of experiments, it was found that E26 transformation specific-1 (ETS1) was a direct target of miR-766 in PDAC cells. Furthermore, ETS1 knockdown simulated the inhibitory effects of the overexpression of miR-766 on PDAC cells, whereas the effects of miR-766 restoration on the PDAC cells were reversed by overexpressing ETS1. In conclusion, the findings of the present study demonstrate that miR-766 offers potential as a therapeutic target for patients with PDAC.

Gastric cancer is one of the most common malignancies in developing countries. We examined the possible role of miR-506 in gastric cancer, investigated its associations with the clinical outcomes of gastric cancer patients, and explored its potential role in angiogenesis and the metastasis of gastric cancer cells. We found that miR-506 expression was a useful marker for stratifying patients from early to advanced clinical stages and for overall survival prediction. miR-506 overexpression inhibited the epithelial-to-mesenchymal transition of gastric cancer cells; however, depletion of miR-506 promoted it. In addition, miR-506 suppressed gastric cancer angiogenesis and was associated with decreased matrix metalloproteinase-9 expression. We also found that ETS1 was a miR-506 target, and it was expressed in 71.10% of gastric cancer tissue samples. Moreover, ETS1 expression was associated with matrix metalloproteinase-9 expression (P < 0.001). In conclusion, miR-506 was identified as an ETS1 targeting suppressor of metastatic invasion and angiogenesis in gastric cancer.