Long non-coding RNA MG3 inhibits proliferation and migration of non-small cell lung carcinoma through regulating EGFR

Lung cancer is the most common and easy to recurrent respiratory tract malignant tumor around the world. Non-small cell lung cancer (NSCLC) shows the highest incidence. Although the molecular targeted therapy becomes a new hot spot, the molecular mechanism underlying the pathogenesis of lung cancer is still unclear. Long noncoding RNA (lncRNA) can participate in the regulation of gene expression through mediating transcription and epigenetics. As a member of lncRNA, maternally expressed gene 3 (MEG3) is involved in various tumors regulation, while its function and related mechanism in NSCLC have not yet been elucidated. Lung cancer cell line A549 and normal bronchial epithelial cell line 16HBE were cultured in vitro. A549 cells were randomly divided into three groups: normal control, empty plasmid group with pcDNA3.1 transfected, and MEG3 group with pcDNA3.1-MEG3 transfected. MEG3 expression was detected by real time PCR. Cell invasive ability was determined by Transwell assay. Cell proliferation was tested by MTT assay. Cell apoptosis was evaluated by flow cytometry. EGFR expression was analyzed by Western blot. Our results showed that MEG3 level significantly declined in A549 cells compared with 16HBE cells (P < 0.05). Compared with control and empty plasmid group, pcDNA3.1-MEG3 plasmid transfection obviously elevated MEG3 expression, suppressed tumor cell proliferation, induced cell apoptosis, declined invasive ability, and downregulated EGFR expression (P < 0.05). In conclusion, LncRNA MEG3 may suppress NSCLC proliferation, promote cell apoptosis, and restrain cell invasion through regulating EGFR. It can be treated as a new biological target for NSCLC diagnosis and treatment.