Influences of LncRNA SNHG20 on proliferation and apoptosis of glioma cells through regulating the PTEN/PI3K/AKT signaling pathway.

  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.