PMID- 28535647
OWN - NLM
STAT- MEDLINE
DCOM- 20170817
LR  - 20181202
IS  - 0253-3766 (Print)
IS  - 0253-3766 (Linking)
VI  - 39
IP  - 5
DP  - 2017 May 23
TI  - [Effects of overexpression of miR-17-92 gene cluster on the biological 
      characteristics of prostate cancer cells and its mechanism].
PG  - 325-331
LID - 10.3760/cma.j.issn.0253-3766.2017.05.002 [doi]
AB  - Objective: To explore the effect and mechanism of over-expression of miR-17-92 
      gene cluster on the biological characteristics of prostate cancer cells. Methods: 
      DU145 cells were transfected with miR-17-92 gene expression plasmid and clones 
      with stable ectopic miR-17-92 overexpression were established. The cell 
      viabilities of DU145-17-92 and DU145-control cells were monitored by xCELLigence 
      system. Cell proliferation and apoptosis were analyzed by Ki-67 and terminal 
      deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Cell cycle was 
      detected by flow cytometry. Expression levels of proteins involved in apoptosis 
      and Akt pathway were determined by western blotting. Results: xCELLigence RTCA 
      array data showed that the growth rate of DU145-17-92 cells was significantly 
      higher than that of DU145-control cells after 24 h of seeding (P<0.01). The 
      Ki-67-positive rates of the DU145-control group at 24, 48 and 72 hours were 
      (56.57+/-1.68)%, (85.48+/-0.26)% and (90.85+/-2.08)%, respectively. While the Ki-67 
      positive rates of the DU145-17-92 group at the desired time points were 
      (73.64+/-0.68)%, (93.43+/-1.23)% and (97.36+/-0.86)%, respectively, with a 
      statistically significant difference at 24 hours (P<0.01). The percentages of 
      apoptotic cells of the DU145-control group at 24, 48 and 72 hours were 
      (6.76+/-0.09)%, (14.51+/-0.86)% and (20.73+/-1.64)%, respectively, while the apoptotic 
      percentages of the DU145-17-92 group were (1.86+/-0.15)%, (7.90+/-0.40)% and 
      (4.92+/-0.48)%, respectively. The percentages of apoptotic cells of the 
      DU145-control group at different time were significantly higher than those of 
      DU145-17-92 group (P<0.01 for all). The result of western blotting showed that 
      the protein expression levels of Bcl-2 interacting mediator of cell death (BIM) 
      and phosphatase and tensin homolog deleted on chromosome ten (PTEN) in 
      DU145-control cells were 0.83+/-0.00 and 0.91+/-0.00, respectively, significantly 
      higher than 0.16+/-0.00 and 0.13+/-0.00 of DU145-17-92 cells (both P<0.01). 
      Overexpression of miR17-92 induced the phosphorylation of protein kinase B (Akt) 
      at Ser473 while no appreciable effect on the phosphorylation of Akt at Thr308. 
      The phosphorylated level of extracellular regulated protein kinases (ERK) in 
      DU145-control cells was 0.21+/-0.01, significantly lower than 0.72+/-0.01 of 
      DU145-17-92 cells (P<0.01). Conclusions: Overexpression of miR-17-92 gene plays a 
      pivotal role in growth, proliferation, apoptosis and cell cycle of DU145 cells 
      through down-regulation of apoptotic protein BIM and tumor suppressor PTEN and 
      activation of Akt and ERK signaling pathway.
FAU - Zhou, P
AU  - Zhou P
AD  - Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 
      215006, China.
FAU - Ma, L
AU  - Ma L
AD  - Jiangsu Institute of Hematology, Suzhou 215006, China.
FAU - Zhou, J
AU  - Zhou J
AD  - Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 
      215006, China.
FAU - Xu, J J
AU  - Xu JJ
AD  - Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 
      215006, China.
FAU - Liu, F
AU  - Liu F
AD  - Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 
      215006, China.
FAU - Guo, F
AU  - Guo F
AD  - Central Laboratory, the First Affiliated Hospital of Soochow University, Suzhou 
      215006, China.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhonghua Zhong Liu Za Zhi
JT  - Zhonghua zhong liu za zhi [Chinese journal of oncology]
JID - 7910681
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (MicroRNAs)
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
MH  - Apoptosis Regulatory Proteins/metabolism
MH  - Cell Cycle
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Down-Regulation
MH  - Gene Expression/*physiology
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Multigene Family/*physiology
MH  - PTEN Phosphohydrolase/metabolism
MH  - Phosphorylation
MH  - Prostatic Neoplasms/genetics/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction
MH  - Time Factors
MH  - Transfection/methods
OTO - NOTNLM
OT  - Bcl-2 interacting mediator of cell death
OT  - Extracellular regulated protein kinases
OT  - Phosphatase and tensin homolog deleted on chromosome ten
OT  - Prostate neoplasms
OT  - Protein kinase B
OT  - miR-17-92
EDAT- 2017/05/26 06:00
MHDA- 2017/08/18 06:00
CRDT- 2017/05/25 06:00
PHST- 2017/05/25 06:00 [entrez]
PHST- 2017/05/26 06:00 [pubmed]
PHST- 2017/08/18 06:00 [medline]
AID - 10.3760/cma.j.issn.0253-3766.2017.05.002 [doi]
PST - ppublish
SO  - Zhonghua Zhong Liu Za Zhi. 2017 May 23;39(5):325-331. doi: 
      10.3760/cma.j.issn.0253-3766.2017.05.002.