To this end, we discuss how nutritional status that leads to an increase of MEG3 expression can protect against cancer and metabolic dysfunctions, while interventions that promote MEG3 downregulation minimize the pleiotropic costs associated with its expression.
However, deregulation of MEG3 is associated with the development and progression of cancer, suggesting that MEG3 may function as a potential biomarker and therapeutic target for human cancers.
Certain polymorphisms within MEG3 are implicated in cancer risk (rs7158663, rs4081134 and rs11160608) or therapeutic response of cancer patients (rs10132552).
Previous studies have revealed that lncRNA maternally expressed gene 3 (MEG3) is involved in the initiation and progression of cancer; however, the underlying mechanisms remain unclear.
Long non-coding RNA (LncRNA) MEG3 serves a regulatory role in the progression of several types of cancer, but the role of MEG3 in laryngeal cancer is still unknown.
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.
Likewise, the long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor that has been shown to regulate cancer cell apoptosis and migration; however, its role in VSMC loss is unclear.
CONCLUSIONS lncRNA AGAP2-AS1 is upregulated in ovarian carcinoma and negatively regulates lncRNA MEG3 to participate in the regulation of cancer cell proliferation.
Importantly, MEG3 was considered as a promising diagnostic biomarker and therapeutic target for patients with osteosarcoma according to the Kaplan-Meier analysis of another independent osteosarcoma data set from the Cancer Genome Atlas (P = 0.05).
Ectopic overexpression of MEG3 using a lentiviral vector Lv-MEG3 significantly inhibited breast cancer cell growth in vitro and a cancer xenograft growth in vivo.
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.
In conclusion, our results demonstrate that only in the pooled analysis, there was a significant relationship between MEG3 expression and cancer survival.
Serum level of MEG3 was lower in cancer patients than that in healthy controls, and the serum level decreased with the increased stage of primary tumor.
It has been proven that maternally expressed 3 (MEG3), a long non-coding RNA (LncRNA), is down-regulated and inversely correlated with prognosis in various types of cancer, including bladder cancer (BC).
Maternally expressed gene 3 (MEG3) is an imprinted gene located at 14q32 which encodes an lncRNA and is downregulated in an expanding list of cancer cell lines and primary human cancers.
The results showed a significant negative association between MEG3 levels and DM (OR = 2.16, 95% CI = 0.99-4.71, P = 0.05, fixed-effect), and it could also predict poor OS (HR = 0.43, 95% CI = 0.15-1.24, P = 0.006, fixed-effect) and RFS (HR = 0.52, 95% CI = 0.29-0.92, P = 0.02, fixed-effect) in cancer patients.
In this study, miR-664a inhibitor was used in order to investigate the changes in the expression levels of MEG3 gene and miR-664a in osteosarcoma cancer cell line (U2-OS) and human osteoblast cell line (hFOB 1.19).
The RT-qPCR technique was used to quantitatively analyze the expression of MEG3 in cancer and adjacent tissues collected from the patients after surgery.
Our findings characterize MEG3 as a tumor suppressive long non-coding RNA in NPC and encourage the development of precise long non-coding RNA-targeted epigenetic therapy against this malignancy.
lncRNA MEG3 has been reported as a tumor suppressor gene in many different kinds of cancer, but its role in gastric cancer has not been fully understood.