调查长链非编码核糖核酸（lncRNA）小核糖核酸宿主基因6（SNHG6）对非小细胞肺癌（NSCLC）细胞增殖和凋亡的影响，并为临床治疗NSCLC提供理论依据。该研究包括25个NSCLC样本和20个正常组织作为实验组。利用荧光定量反转录-聚合酶链反应（qRT-PCR）检测lncRNA SNHG6和p21。统计分析NSCLC组织中lncRNA SNHG6和p21之间的关系。利用集落形成实验和流式细胞术确定细胞周期分布和细胞凋亡。使用甲基噻唑酰四唑（MTT）法确定细胞增殖，使用Western blotting（WB）测定p21的蛋白表达。NSCLC组织的SNHG6表达水平[(1.98 ± 0.23) vs. (4.46 ± 0.52)]（P < .01）显著增高，但p21表达[(1.02 ± 0.23) vs. (0.33 ± 0.15)]（P < .01）更低。SNHG6的表达与p21呈负相关（r2 = 0.2173，P = .0188）。在HCC827和H1975细胞中转染SNHG6小干扰RNA（siRNA）（si-SNHG6）显着降低了SNHG6水平。转染pcDNA-SNHG6的BEAS-2B细胞比正常细胞具有更强的增殖和集落形成能力（P < .01）。SNHG6的上调促进了BEAS-2B细胞的恶性表型和增殖能力。通过影响凋亡和p21表达，在SNHG6敲降后，HCC827和H1975细胞的增殖、集落形成能力和G1期的细胞周期显著受到抑制（P < .01）。沉默lncRNA SNHG6通过调控p21抑制了NSCLC细胞的增殖并促进凋亡。

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.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.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).Silencing lncRNA SNHG6 represses the proliferation and facilitates the apoptosis of NSCLC cells through regulating p21.