Knock down of SIRLNT by Antisense LNA GapmeRs and evaluation of its inhibitory effect on proliferation in human breast cancer cells

Introduction and Objectives: long non-coding RNAs (lncRNAs) play a critical role in progression of human disease especially in cancer. LncRNAs being potential candidates for therapeutical applications during different diseases. In caccer, lncRNAs could be as either oncogenes or tumor suppressor genes. In the current study, we targeted oncogenic lncRNA SIRLNT (SIRT1 regulating lncRNA tumor promoter) as one of the most significantly up-regulated lncRNA in human breast cancer.Materials and Methods: We used Antisense locked nucleic acid (LNA) GapmeRs oligonucleotides method, which is a potent transduction system to regulate lncRNA SIRLNT expression. MCF-7 cell line was transfected with lncRNA-SIRLNT antisense LNA GapmeRs at three different time points. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to evaluate expression of lncRNA-SIRLNT and SIRT1 (as a molecule under the influence of lncRNA-SIRLNT). The effects of lncRNA-SIRLNT knock down on cell proliferation were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.Results: The results suggest that lncRNA SIRLNT was significantly downregulated and SIRT1 upregulated significantly after transfection MCF-7 cell line by Antisense LNA GapmeRs. Significantly, we found that the LncRNA SIRLNT knockdown lead to reduction of proliferation of MCF-7 cell line.Conclusion: Our finding suggests that lncRNA SIRLNT inhibition could be a promising therapeutic approach to prevent progression of breast cancer.

کلیدواژه ها:

Breast cancer ، LncRNA SIRLNT ، LNA GapmeRs oligonucleotides ، MCF-7 ، Sirtuin1