The results indicated that MEG3 levels were positively correlated with GH and IGF-1 levels, and negatively correlated with the tumor volume of GH-secreting tumors.
As a classical long noncoding RNA (lncRNA), maternally expressed gene 3 (MEG3) has been reported to exhibit pivotal regulatory roles in the occurrence and development of various digestive system tumors.
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.
The long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3), a tumor suppressor, is critical for the carcinogenesis and progression of different cancers, including hepatocellular carcinoma (HCC).
Here, we found that MEG3 expression was significantly downregulated in tumour tissues, and its low expression was associated with large tumour size, lymph node metastasis and advanced clinical stage in ESCC patients.
To conclude, as our findings proved, MEG3 is likely to act as a tumor suppressor in the pathogenesis of CRC by means of the regulation of the miR-376/PRDK1 signal axis, suggesting that MEG3 has the potential to become a novel therapeutic target for the treatment of CRC.
The present review highlights biological function of MEG3 to repress tumor through regulating the major tumor suppressor genes p53 and Rb, inhibiting angiogenesis-related factor, or controlling miRNAs.
The present study also revealed that lncRNA‑MEG3 transfection suppressed tumor growth mainly by decreasing the expression of vascular endothelial growth factor and increasing the expression of Bcl‑2 in vivo.
MTT, colony formation assay, flow cytometry analysis and a subcutaneous xenograft tumor model were conducted to assess the effects of MEG3 on the HAs tumorigenesis.