Enhanced expression of non coding miR 92a expression is implicated in the development of lung cancer.

Abstract

MicroRNAs (miRNAs/miRs) are small noncoding RNAs that primarily function in RNA silencing and gene regulation at the posttranscriptional level in animals, plants and certain viruses. They have been reported to play a vital role in development and progression of diseases such as cancer. The present study was undertaken to establish a correlation between a specific miRNA in this cluster, termed miR92a, and its association with nonsmall cell lung cancer (NSCLC). Total RNA was isolated from the plasma using an RNeasy mini kit and cDNA was synthesized by TaqMan MicroRNA Reverse Transcription kit. The expression of miR-92a was quantified by quantitative Real-time PCR (RT-PCR). All transfections were performed using Lipofectamine 2000. Digoxigenin (DIG)labeled locked nucleic acid (LNA)modified probes for miR92a and negative control oligonucleotides were used for in vitro hybridization following manufacturers protocol. Digoxigenin (DIG)labeled locked nucleic acid (LNA)modified probes for miR92a and negative control oligonucleotides (miRCURY LNA MicroRNA Detection Probes; Exiqon, Vedbaek, Denmark) were used. Cell proliferation was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) MTT assay. It was observed that miR92a is highly expressed in NSCLC compared with adjacent tissue samples and plasma from healthy donors. Additionally, the proliferation of three NSCLCderived cell lines, SPCA1, A549 and H2170, was enhanced by miR92a and inhibited by a complementary antimiR92a oligonucleotide sequence. Although the underlying mechanisms of reduced cellular proliferation in the presence of miR92a antagomirs cannot be explained from the current results. The upregulation of miR92a expression, in cells and plasma, is manifested during the development of NSCLC.