PMID- 30657567
OWN - NLM
STAT- MEDLINE
DCOM- 20200619
LR  - 20200619
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 1
DP  - 2019 Jan
TI  - Influences of LncRNA SNHG20 on proliferation and apoptosis of glioma cells 
      through regulating the PTEN/PI3K/AKT signaling pathway.
PG  - 253-261
LID - 16771 [pii]
LID - 10.26355/eurrev_201901_16771 [doi]
AB  - OBJECTIVE:   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. PATIENTS AND METHODS: 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. RESULTS: 
      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). CONCLUSIONS: 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.
FAU - Guo, L-P
AU  - Guo LP
AD  - Department of Neurosurgery, Shouguang People's Hospital of Shandong, Weifang, 
      China. svgz66@163.com.
FAU - Zhang, Z-J
AU  - Zhang ZJ
FAU - Li, R-T
AU  - Li RT
FAU - Li, H-Y
AU  - Li HY
FAU - Cui, Y-Q
AU  - Cui YQ
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (long non-coding RNA SNHG20, human)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (PTEN protein, human)
SB  - IM
MH  - Apoptosis/genetics
MH  - Brain/pathology/surgery
MH  - Brain Neoplasms/*genetics/pathology/surgery
MH  - Carcinoma/*genetics/pathology/surgery
MH  - Cell Line, Tumor
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Gene Knockout Techniques
MH  - Glioma/*genetics/pathology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - PTEN Phosphohydrolase/metabolism
MH  - Phosphatidylinositol 3-Kinase/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Long Noncoding/genetics/*metabolism
MH  - RNA, Messenger/metabolism
MH  - RNA, Small Interfering/metabolism
MH  - Signal Transduction/genetics
EDAT- 2019/01/19 06:00
MHDA- 2020/06/20 06:00
CRDT- 2019/01/19 06:00
PHST- 2019/01/19 06:00 [entrez]
PHST- 2019/01/19 06:00 [pubmed]
PHST- 2020/06/20 06:00 [medline]
AID - 16771 [pii]
AID - 10.26355/eurrev_201901_16771 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):253-261. doi: 
      10.26355/eurrev_201901_16771.