LncRNA HOTAIR Promotes Proliferation of Malignant Mela-noma Cells Through NF-κB Pathway

Background: to study the effects of long non-coding ribonucleic acid (lncrna) hox transcript antisense intergenic rna (hotair) on the proliferation and apoptosis of malignant melanoma cells, and to explore its specific regulatory mechanism through the nuclear factor-κb (nf-κb) signaling pathway. methods: lncrna hotair small-interfering rnas (sirnas) were designed and synthesized, and the effects of si-hotair transfection on the proliferation and apoptosis of malignant melanoma cells were detected via cell counting kit-8 (cck-8) assay, 4',6-diamidino-2-phenylindole (dapi) staining assay and flow cytometry, respectively. the gene expressions were determined using quantitative reverse transcription-polymerase chain reaction (qrt-pcr), the changes in nf-κb pathway-related proteins and apoptosis-associated proteins after interference in lncrna hotair were detected via western blotting, and the level of nf-κb in each group was determined via elisa. results: the results of cck-8 assay revealed that the cell proliferation rate significantly declined gradually in si-hotair group compared with that in si-nc group and control group (p<0.05). the results of western blotting and elisa showed that the activity of nf-κb in si-hotair group was weakened (p<0.05), suggesting that down-regulation of hotair can suppress the activity of nf-κb. compared with si-nc group and control group, si-hotair group had remarkably increased gene and protein expressions of pro-apoptotic bax, and remarkably decreased gene and protein expressions of anti-apoptotic bcl-2 (p<0.05), demonstrating that down-regulation of hotair can promote apoptosis. conclusion: down-regulation of lncrna hotair can inhibit the proliferation and promote the apoptosis of malignant melanoma cells and suppress the nf-κb pathway.