MEG3 over-expression suppressed cell viability, colony formation, cell invasion and migration of PC3 cells in vitro and inhibited tumorigenesis of PC3 cells in vivo, while EN2 over-expression diminished the effects.
We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-β inhibitor treatment reduced those enhancing effects.
It was demonstrated that lncRNA‑MEG3 expression was downregulated in gastric carcinoma cells compared with normal gastric cells. lncRNA‑MEG3 transfection increased E‑cadherin expression and markedly inhibited gastric carcinoma cell growth, migration and invasion.
In addition, rescue experiments demonstrated that overexpression of AP1G1 partially reversed the promotive effect of lowly-expressed MEG3 on cell proliferation and invasion, suggesting that low expression of MEG3 may activate PI3K/AKT pathway by inhibiting AP1G1 expression.
The overexpression of MEG3 and the application of 5-Aza treatment inhibited the migration, invasion and proliferation of MGC-803 cells and promoted apoptosis.
Further analysis demonstrated that lncRNA MEG3 overexpression significantly inhibited HTR-8/SVneo cell viability, and prevented cell migration and invasion in addition to inducing cell apoptosis.
The upregulated MEG3 and miR-361-5p or the downregulated FoxM1 appeared to substantially inhibit proliferation, migration, and invasion of osteosarcoma cells (p < 0.05).
Furthermore, our results showed that MEG3 interacted with miR-184 and subsequently mitigated the proliferation and invasion of leukemia cells by downregulating related proteins.
Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis.
MEG3 knockdown enhanced cell proliferation, promoted cell migration and invasion, induced epithelial‑mesenchymal transition (EMT), increased the sphere‑forming ability and cancer stem cell (CSC) properties, and decreased the chemosensitivity to gemcitabine in vitro.