长链非编码 RNA SNHG6 通过靶向 P21 在非小细胞肺癌细胞中的生物学作用。
The Biological Role of Lncrna SNHG6 in Non-Small Cell Lung Cancer Cells Via Targeting P21.
出版信息
Altern Ther Health Med. 2023 May;29(4):158-163.
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.
目的
研究长链非编码核糖核酸（lncRNA）小核仁 RNA 宿主基因 6（SNHG6）对非小细胞肺癌（NSCLC）细胞增殖和凋亡的影响，为 NSCLC 的临床治疗提供理论依据。
方法
本研究纳入 25 例 NSCLC 组织标本和 20 例正常组织作为实验组。采用荧光定量逆转录聚合酶链反应（qRT-PCR）检测 lncRNA SNHG6 和 p21 的表达。统计分析 NSCLC 组织中 lncRNA SNHG6 与 p21 的关系。采用集落形成实验和流式细胞术检测细胞周期分布和细胞凋亡。噻唑蓝（MTT）比色法检测细胞增殖，Western blot（WB）检测 p21 蛋白表达。
结果
25 例 NSCLC 组织中 SNHG6 的表达水平[（1.98±0.23）比（4.46±0.52）]（P<0.01）显著升高，而 p21 的表达水平[（1.02±0.23）比（0.33±0.15）]（P<0.01）明显降低。SNHG6 的表达与 p21 呈负相关（r2=0.2173，P=0.0188）。在 HCC827 和 H1975 细胞中转染 SNHG6 小干扰 RNA（si-SNHG6）可显著降低 SNHG6 的表达水平。转染 pcDNA-SNHG6 的 BEAS-2B 细胞的活力比正常细胞更具增殖和集落形成能力（P<0.01）。上调 SNHG6 可促进 BEAS-2B 细胞的恶性表型形成和增殖能力。敲低 SNHG6 后，HCC827 和 H1975 细胞的增殖、集落形成能力和细胞周期 G1 期明显受到抑制，同时影响细胞凋亡和 p21 的表达（P<0.01）。
结论
沉默 lncRNA SNHG6 通过调节 p21 抑制 NSCLC 细胞的增殖并促进其凋亡。
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