For figuring out the effect of MEG3 in breast cancer cells MCF7 and MB231, we overexpressed MEG3 in these cells, and found that it resulted the inhibition of proliferation, colony formation, migration and invasion capacities by enhancing p53's transcriptional activity on its target genes, including p21, Maspin and KAI1.
As expected, luciferase results verified the putative target site and also revealed the complementary binding between miR-19a and MEG3. miR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration, and invasion.
Overexpression of MEG3 inhibited breast cancer cell proliferation and invasion, suggesting that MEG3 played an important role in breast cancer progression and metastasis.
Furthermore, our results showed that MEG3 interacted with miR-184 and subsequently mitigated the proliferation and invasion of leukemia cells by downregulating related proteins.
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.
We further observed the impact of MEG3 on the invasion and migration functions of human trophoblast cells and the effects on EMT and TGF-β/smad signaling pathways in an Human trophoblast cell-8 (HTR-8)Vneo cell line.
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.
MiR-7, directly binding to MEG3, was overexpressed in the CCRCC tissues and could inhibit the apoptosis and promote the migration and invasion of CCRCC cells.
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).
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.
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.