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: LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer.
    Author: Zhang W, Shi S, Jiang J, Li X, Lu H, Ren F.
    Journal: Biomed Pharmacother; 2017 Jul; 91():312-319. PubMed ID: 28463794.
    Abstract:
    BACKGROUND: MEG3, a lncRNA, has been verified in several tumors to function as tumor suppressors including breast cancer development and progression, however, the expression pattern and underlying mechanisms of MEG3 involved in breast cancer progression is still need to be further explored. METHODS: The expression of MEG3 was confirmed in 90 cases of breast cancer tissues compared to adjacent normal tissues by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The association between clinicopathological factors and MEG3 expression was evaluated by chi-square test. Kaplan-Meier curve and log rank test was performed to assess disease-free survival (DFS) and overall survival (OS) time in patients. CCK8 and transwell invasion assays were used to assess cell proliferation and invasion capacity. Luciferase report assay and RNA pull down assay were used to detect the association between miR-421 and MEG3 in breast cancer. RESULTS: In the study, we demonstrated that the expression of MEG3 was significantly down-regulated in breast cancer tissues compared to adjacent normal tissues. Reducing MEG3 expression was significantly associated with TNM stage and lymph nodes metastasis in patients. Survival analysis showed that lower MEG3 predicted a poor DFS and OS for patients. In vitro, we showed that up-regulated MEG3 inhibited cell proliferation and cell invasion capacities. We further revealed that endogenous miR-421 expression was negatively regulated by MEG3 in breast cancer cells and MEG3 regulated E-cadherin expression by sponging to miR-421 in breast cancer cells. CONCLUSIONS: Our results showed that MEG3/miR-421/E-cadherin regulatory axis may be a novel therapeutic target for breast cancer.
    [Abstract] [Full Text] [Related] [New Search]