Concurrent Targeting of MEG3 and Linc-ROR Increases the p53 Transcript in HCT116 Cells

Abstract Recently, lncRNAs are used as a prospective strategy in cancer gene therapy. Dysregulation of the maternally expressed gene3 (MEG3) and the linc-ROR have demonstrated in colorectal cancer researches. This study evaluates the effect of concurrent silencing of linc-ROR and MEG3 activation on colon cancer cell survival in order to assess the p53 transcriptional activity and stability. The MEG3 and linc-ROR shRNA were cloned under the bidirectional CEA promoter (UM1). Transfection efficiency was examined by GFP expression under fluorescent microscope. Following transfection, the response of HCT116 cells was evaluated by MTS assay, apoptosis and cell cycle analyses. The expression of target genes along with the p53 were analyzed in the transcription level by qPCR.Proliferation of both cancer cell lines were significantly reduced at 48 h post-transfection. The UM1 significantly induced apoptosis in HCT116 (36.35%). Moreover, UM1 remarkably reduced the cell population in S phase. Also, concomitant up- and down-regulation of MEG3 and linc-ROR were attributed to the activation of p53 in transcription level. Concurrent silencing of linc-ROR and MEG3 activation in colon cancer cells resulted in the activation of p53 and reduced the cell proliferation. We found that the higher apoptosis induction was coupled with the enhancement of the p53 expression. The synergistic effect of target genes might serve as a useful approach for targeting p53 in colon cancer.