Altern Ther Health Med. 2023 Mar 20:AT7962. Online ahead of print.
OBJECTIVE: To investigate the influence of long non-coding ribonucleic acid (lncRNA) small nucleolar RNA host gene 6 (SNHG6) on proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and to provide a theoretical basis for the clinical treatment of NSCLC.
METHODS: This study included 25 samples of NSCLC and 20 normal tissues as the experimental group. Fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect lncRNA SNHG6 and p21. The relationship between lncRNA SNHG6 and p21 in NSCLC tissues was analyzed statistically. Colony formation assay and flow cytometry were used to determine the cell cycle distribution and cell apoptosis. Methyl thiazolyl tetrazolium (MTT) assay was used to determine cell proliferation, and Western blotting (WB) was used to measure the protein expression of p21.
RESULTS: The expression level of SNHG6 [(1.98 ± 0.23) vs. (4.46 ± 0.52)] (P < .01) was significantly higher, but p21 expression [(1.02 ± 0.23) vs. (0.33 ± 0.15)] (P < .01) was lower in the 25 cases of NSCLC tissues than in the control group. The expression of SNHG6 was negatively correlated with p21 (r2 = 0.2173, P = .0188). Transfection of SNHG6 small interfering RNA (siRNA) (si-SNHG6) in HCC827 and H1975 cells significantly reduced the level of SNHG6. The viability of BEAS-2B cells transfected with pcDNA-SNHG6 had a more robust proliferative and colony-forming capacity than normal cells (P < .01). Up-regulation of SNHG6 promoted the formation of the malignant phenotype and proliferative capacity of BEAS-2B cells. Proliferation, colony-forming capacity, and G1 phase of the cell cycle in HCC827 and H1975 cells were significantly repressed via influencing the apoptosis and p21 expression after the knockdown of SNHG6 (P < .01).
CONCLUSION: Silencing lncRNA SNHG6 represses the proliferation and facilitates the apoptosis of NSCLC cells through regulating p21.