These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: MicroRNA‑766 inhibits the malignant biological behaviours of pancreatic ductal adenocarcinoma by directly targeting ETS1.
    Author: Li S, Yan G, Yue M, Kang Z, Wang L.
    Journal: Mol Med Rep; 2019 Feb; 19(2):1380-1387. PubMed ID: 30569091.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]