This study was aimed to figure out whether long noncoding RNA MEG3/miR-361-5p/FoxM1 signaling would contribute to improved proliferation and metastasis of osteosarcoma cells.
Additionally, microRNA‑96‑5p (miR‑96‑5p) was a promising target of MEG3, and the promoting effects of miR‑96‑5p on cell growth and metastasis could be reversed by upregulated MEG3.
This study evaluated the expression of lncRNA MEG3 and a microRNA (miRNA-10a-5p) implicated in HCC metastasis in cancer and carcinoma adjacent tissues of HCC samples (n=30 each) via in situ hybridization and quantitative RT-PCR.
Wound healing, transwell, colony formation and flow cytometry assays were used to analyze the effects of lncRNA MEG3 and methylation on tumor cell migration, invasion, proliferation and apoptosis.
Dysregulation of long noncoding RNAs (lncRNAs) is associated with the proliferation and metastasis in a variety of cancers, of which lncRNA maternally expressed gene 3 (MEG3) has been indicated as a tumor suppressor in multiple malignancies.
Using a mouse xenograft tumor model, we found that the overexpression of MEG3 suppressed tumor growth and metastasis while overexpression of miR‑21 had the opposite effects.
In further, Clusterin over-expression rescues the compromised abilities of proliferation and metastasis induced by MEG3 over-expression, suggesting that MEG3 inhibits the CRC progression through regulating the Clusterin activities.
Overexpression of MEG3 inhibited breast cancer cell proliferation and invasion, suggesting that MEG3 played an important role in breast cancer progression and metastasis.
Finally, we observed that EWSAT1 facilitates OS cell growth and metastasis through regulation of MEG3, suggesting that EWSAT1-MEG3 axis might be a promising target for OS treatment.
The results showed that MEG3 was downregulated in retinoblastoma tissues, and the level of MEG3 was negatively associated with IIRC stages and nodal or distant metastasis.