Investigation of cell proliferation of MALAT1 (Long non coding RNA) in lung cancer

Lung cancer is the second most frequently observed cancer type and is mostly responsible for cancer deaths in males. Many environmental factors that can cause lung cancer such as non-coding RNAs (lncRNAs) whıch are undısputed ın lung cancers. Long noncoding RNAs have been studied in many cancers and have been found to be responsible for metastasis, cell proliferation and invasion in several cancer types. The long noncoding RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), is a highly conserved nuclear noncoding RNA (ncRNA) and a predictive marker for metastasis and cell proliferation development in lung cancer. Therefore a lncRNA, MALAT1 has been selected for their gene expression studies and for the investigation of MALAT1 as a possible biomarker in diagnosis. It is to be thought that after the downregulation of MALAT1 expression, the alternative splice variant factors of B-MYB control cell proliferation in lung cancer via rearrangement. Taking these in considerations we used Real-Time PCR in order to find out the expression level of MALAT1 and B-MYB in lung cancer cell line (A549). We used flow cytometry to determine the effect in cell proliferation and the level of apoptosis in G2/M. There was a significant decrease in gene expression of MALAT1 and B-MYB in cell line using miR-503 as compared to cell line with negatif kontrol miRNA, miR-150 and miR-15a. When we analysed cell proliferation and apoptosis, there was an increase in the number of cells undergoing apoptosis while there was decrease in the number of cells entering G2/M phase of cell cycle in cells with miR-503 as compared to cells with other miRNAs. As a result it can be concluded that miR-503 and miR-150 has a role in MALAT1 expression, cell proliferation and apoptosis by targeting MALAT1 and has been found to decrease cell proliferation and increase apoptosis of lung cancer cell line.