PMID- 27176210
OWN - NLM
STAT- MEDLINE
DCOM- 20170406
LR  - 20220316
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 14
IP  - 1
DP  - 2016 Jul
TI  - (‑)‑Epigallocatechin‑3‑gallate induces apoptosis in human pancreatic cancer cells 
      via PTEN.
PG  - 599-605
LID - 10.3892/mmr.2016.5277 [doi]
AB  - Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a cancer 
      suppressor gene and an important negative regulator in the phosphatidylinositide 
      3‑kinase (PI3K)/protein kinase B (Akt)/ mechanistic target of rapamycin (mTOR) 
      signaling pathway. The PI3K/Akt/mTOR pathway can promote cancer cell survival, 
      proliferation and progression. In the present study, the effects of 
      (‑)‑epigallocatechin‑3‑gallate (EGCG) on PI3K/Akt/mTOR signaling in pancreatic 
      cancer cells and PTEN knockdown cells were measured, in addition to assessing its 
      therapeutic potential in pancreatic cancer. The apoptosis and proliferation of 
      the cancer cells were examined by flow cytometry and Cell Counting kit‑8 assay, 
      respectively. The expression of genes and proteins in the PI3K/Akt/mTOR signaling 
      pathway were investigated by reverse transcription‑polymerase chain reaction and 
      western blotting, respectively. The results suggested that the EGCG‑induced 
      apoptosis, proliferation inhibition and downregulated expression of 
      phosphorylated (p)‑Akt and p‑mTOR were partially attenuated in PTEN‑knockdown 
      cells. In conclusion, the results indicated that EGCG is able to reduce 
      proliferation and induce the apoptosis of pancreatic cancer cells associated with 
      the expression of PTEN. Additionally, EGCG can suppress the expression of p‑Akt 
      and p‑mTOR via PTEN to regulate the PI3K/Akt/mTOR pathway. The results suggest 
      that EGCG may represent a potential treatment for pancreatic cancer, based on 
      PTEN activation.
FAU - Liu, Shi
AU  - Liu S
AD  - Department of General Surgery, The Third Affiliated Hospital of Qiqihar Medical 
      University, Qiqihar, Heilongjiang 161099, P.R. China.
FAU - Xu, Zhong-Ling
AU  - Xu ZL
AD  - Department of Oncology, The Third Affiliated Hospital of Qiqihar Medical 
      University, Qiqihar, Heilongjiang 161099, P.R. China.
FAU - Sun, Li
AU  - Sun L
AD  - Department of Oncology, The Third Affiliated Hospital of Qiqihar Medical 
      University, Qiqihar, Heilongjiang 161099, P.R. China.
FAU - Liu, Ying
AU  - Liu Y
AD  - Department of Oncology, The Third Affiliated Hospital of Qiqihar Medical 
      University, Qiqihar, Heilongjiang 161099, P.R. China.
FAU - Li, Cheng-Chong
AU  - Li CC
AD  - Department of Pharmaceutical Science, Qiqihar Medical University, Qiqihar, 
      Heilongjiang 161099, P.R. China.
FAU - Li, Hong-Mei
AU  - Li HM
AD  - Department of Pharmaceutical Science, Qiqihar Medical University, Qiqihar, 
      Heilongjiang 161099, P.R. China.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Oncology, The Third Affiliated Hospital of Qiqihar Medical 
      University, Qiqihar, Heilongjiang 161099, P.R. China.
FAU - Li, Cheng-Jun
AU  - Li CJ
AD  - Department of Pharmaceutical Science, Qiqihar Medical University, Qiqihar, 
      Heilongjiang 161099, P.R. China.
FAU - Qin, Wei
AU  - Qin W
AD  - Department of Pharmaceutical Science, Qiqihar Medical University, Qiqihar, 
      Heilongjiang 161099, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20160513
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (RNA, Small Interfering)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
SB  - IM
MH  - Apoptosis/*drug effects/genetics
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cell Proliferation/drug effects
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - PTEN Phosphohydrolase/genetics/*metabolism
MH  - Pancreatic Neoplasms/genetics/*metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA Interference
MH  - RNA, Small Interfering
MH  - Signal Transduction/drug effects
EDAT- 2016/05/14 06:00
MHDA- 2017/04/07 06:00
CRDT- 2016/05/14 06:00
PHST- 2015/05/28 00:00 [received]
PHST- 2016/04/06 00:00 [accepted]
PHST- 2016/05/14 06:00 [entrez]
PHST- 2016/05/14 06:00 [pubmed]
PHST- 2017/04/07 06:00 [medline]
AID - 10.3892/mmr.2016.5277 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Jul;14(1):599-605. doi: 10.3892/mmr.2016.5277. Epub 2016 May 
      13.