Department of Neurosurgery, Shouguang People's Hospital of Shandong, Weifang, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):253-261. doi: 10.26355/eurrev_201901_16771.
To investigate the influences of long non-coding ribonucleic acid (lncRNA) small nucleolar RNA host gene 20 (SNHG20) on proliferation and apoptosis of glioma cells, and further explore the mechanism of SNHG20 in the incidence and development of glioma.
A total of 80 cases of glioma specimens and 80 cases of para-carcinoma specimens were collected, and the expression level of SNHG20 was detected via reverse transcription-polymerase chain reaction (RT-PCR). The human glioma U118 and U251 cell lines with the stable knockout of SNHG20 were constructed using the small-interfering RNA (siRNA). The influence of SNHG20 on proliferation of human glioma cells was detected via cell counting kit-8 (CCK-8), and the protein expression levels of apoptosis-related genes, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax), were also detected. The apoptosis level of glioma cells was detected in blank control group and SNHG20 siRNA group using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) technique. At the same time, the expression levels of proteins related to the phosphatase and tensin homolog deleted on chromosome ten/phosphatidylinositol 3-hydroxy kinase/protein kinase B (PTEN/PI3K/AKT) signaling pathway were detected via Western blotting.
The expression level of SNHG20 messenger RNA (mRNA) in glioma tissues was significantly higher than that in para-carcinoma tissues (p<0.05). After the inhibition of siRNA on SNHG20, the proliferation of U118 and U251 cells was significantly inhibited, and the expression of Bax was significantly up-regulated, while that of Bcl-2 was down-regulated. The TUNEL results showed that the number of apoptotic cells in SNHG20 siRNA group was about 12 times that in control group (p<0.05). After SNHG20 knockout, the protein expressions in the PTEN/PI3K/AKT signaling pathway were inhibited (p<0.05).
Inhibiting the SNHG20 expression in glioma cells can increase the apoptosis of glioma cells, and the mechanism may be related to the SNHG20-mediated PTEN/PI3K/AKT signaling pathway.
研究长链非编码核糖核酸（lncRNA）小核仁 RNA 宿主基因 20（SNHG20）对神经胶质瘤细胞增殖和凋亡的影响，并进一步探讨 SNHG20 在神经胶质瘤发病和发展中的机制。
收集 80 例神经胶质瘤标本和 80 例癌旁标本，采用逆转录-聚合酶链反应（RT-PCR）检测 SNHG20 的表达水平。构建了稳定敲除 SNHG20 的人神经胶质瘤 U118 和 U251 细胞系，采用小干扰 RNA（siRNA）。通过细胞计数试剂盒-8（CCK-8）检测 SNHG20 对人神经胶质瘤细胞增殖的影响，检测凋亡相关基因 B 细胞淋巴瘤-2（Bcl-2）和 Bcl-2 相关 X 蛋白（Bax）的蛋白表达水平。用末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）技术检测空白对照组和 SNHG20 siRNA 组神经胶质瘤细胞的凋亡水平。同时，采用 Western blot 检测磷酸酶和张力蛋白同源物缺失于染色体 10/磷脂酰肌醇 3-激酶/蛋白激酶 B（PTEN/PI3K/AKT）信号通路相关蛋白的表达水平。
神经胶质瘤组织中 SNHG20 信使 RNA（mRNA）的表达水平明显高于癌旁组织（p<0.05）。siRNA 抑制 SNHG20 后，U118 和 U251 细胞的增殖明显受到抑制，Bax 的表达明显上调，Bcl-2 的表达下调。TUNEL 结果显示，SNHG20 siRNA 组凋亡细胞数约为对照组的 12 倍（p<0.05）。SNHG20 敲除后，PTEN/PI3K/AKT 信号通路中的蛋白表达受到抑制（p<0.05）。
抑制神经胶质瘤细胞中的 SNHG20 表达可增加神经胶质瘤细胞的凋亡，其机制可能与 SNHG20 介导的 PTEN/PI3K/AKT 信号通路有关。
