PMID- 38462356
OWN - NLM
STAT- MEDLINE
DCOM- 20240312
LR  - 20240312
IS  - 0376-2491 (Print)
IS  - 0376-2491 (Linking)
VI  - 104
IP  - 10
DP  - 2024 Mar 12
TI  - [LncRNA SNHG11 promotes malignant progression of colorectal cancer cells through 
      the PI3K/Akt/mTOR signaling pathway].
PG  - 758-765
LID - 10.3760/cma.j.cn112137-20231103-00998 [doi]
AB  - Objective: To investigate the effects of lncRNA SNHG11 on proliferation, 
      migration, invasion and apoptosis of colorectal cancer cancer cells and possible 
      mechanisms. Methods: qRT-PCR was performed to detect the expression level of 
      lncRNA SNHG11 in colorectal cancer tissues and its related cell lines. The 
      correlation between SNHG11 expression and clinical prognosis of patients was 
      assessed by bioinformatics techniques. Cultured CRC cell lines were transfected 
      with shCtrl (shCtrl group), shSNHG11#1 (shSNHG11#1 group), shSNHG11#2 (shSNHG11#2 
      group), Control cDNA (Control cDNA group), and SNHG11 cDNA (SNHG11 cDNA), 
      respectively. Thiazolyl blue (MTT), clone formation assay, Transwell assay, cell 
      scratch assay, and flow cytometry were used to detect the proliferation, 
      migration, invasion, and apoptosis of CRC cells in each group. Western protein 
      blotting was used to detect the expression of relevant proteins in each group, 
      and the effect of lncRNA SNHG11 knockdown on the growth of tumour cells in vivo 
      was analysed by nude mice tumouring assay. Phosphatidylinositol 3-kinase 
      (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signalling 
      pathway inhibitor LY294002 was used for rescue experiments. Results: The 
      expression of lncRNA SNHG11 was significantly higher in colorectal cancer cells 
      and tissues than in normal tissues (P<0.05). Survival analysis showed that the 
      expression level of SNHG11 was not statistically associated with CRC survival 
      (P>0.05). shSNHG11#2 group compared with shCtrl group. MTT OD490/570 values 
      decreased, the number of CRC cell clones decreased, the number of Transwell cells 
      decreased, the area of cell scratch decreased, and the apoptosis rate increased 
      (P<0.05). The mesenchymal markers matrix metalloproteinase (MMP9), N-cadherin and 
      vimentin were significantly reduced, and the expression of the epithelial marker 
      E-cadherin was upregulated. The expression of anti-apoptotic proteins Bcl-2 and 
      Bcl-xl was decreased, and the expression of pro-apoptotic protein Bax was 
      increased (P<0.05).In vivo experiments showed that lncRNA SNHG11 knockdown 
      inhibited the growth of colorectal cancer cells, and the expression of Ki67 was 
      reduced in tumours (P<0.05). LncRNA SNHG11 knockdown inhibited the expression of 
      p-PI3K, p-Akt and p-mTOR.The PI3K/Akt/mTOR signaling pathway inhibitor LY294002 
      was able to restore the malignant cytological progression of colorectal cancer 
      cells induced by the overexpression of lncRNA SNHG11. Conclusions: LncRNA SNHG11 
      is highly expressed in colorectal cancer. lncRNA SNHG11 can promote the malignant 
      progression of colorectal cancer cells by regulating the PI3K/Akt/mTOR signaling 
      pathway, and this finding provides a new theoretical basis for targeted therapy 
      of colorectal cancer.
FAU - Tao, S N
AU  - Tao SN
AD  - Department of Nuclear Medicine, the First Affiliated Hospital of Wannan Medical 
      College,Wuhu 241000, China.
FAU - Liu, X C
AU  - Liu XC
AD  - Department of Nuclear Medicine, the First Affiliated Hospital of Wannan Medical 
      College,Wuhu 241000, China.
FAU - Wang, Y Y
AU  - Wang YY
AD  - Department of Nuclear Medicine, the First Affiliated Hospital of Wannan Medical 
      College,Wuhu 241000, China.
FAU - Yang, H
AU  - Yang H
AD  - Central Laboratory,Anhui Province Key Laboratory of Non-coding RNA Basic and 
      Clinical Transformation,the First Affiliated Hospital of Wannan Medical 
      College,Wuhu 241000, China.
LA  - chi
GR  - RNA202006/The Opening Foundation of Key Laboratory of Non-coding RNA 
      Transformation Research of Anhui Higher Education Institution/
GR  - 2023AH051746/Key University Science Research Project of Anhui Province/
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhonghua Yi Xue Za Zhi
JT  - Zhonghua yi xue za zhi
JID - 7511141
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (DNA, Complementary)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Humans
MH  - Phosphatidylinositol 3-Kinase/metabolism/pharmacology
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Phosphatidylinositol 3-Kinases/genetics/metabolism/pharmacology
MH  - *RNA, Long Noncoding/genetics
MH  - Mice, Nude
MH  - DNA, Complementary/pharmacology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/genetics/metabolism/pharmacology
MH  - *Colorectal Neoplasms/genetics
MH  - Mammals/genetics/metabolism
EDAT- 2024/03/11 00:42
MHDA- 2024/03/12 06:42
CRDT- 2024/03/10 22:18
PHST- 2024/03/12 06:42 [medline]
PHST- 2024/03/11 00:42 [pubmed]
PHST- 2024/03/10 22:18 [entrez]
AID - 10.3760/cma.j.cn112137-20231103-00998 [doi]
PST - ppublish
SO  - Zhonghua Yi Xue Za Zhi. 2024 Mar 12;104(10):758-765. doi: 
      10.3760/cma.j.cn112137-20231103-00998.