Abstract:
: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.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Liu S,Xu ZL,Sun L,Liu Y,Li CC,Li HM,Zhang W,Li CJ,Qin Wdoi
10.3892/mmr.2016.5277subject
Has Abstractpub_date
2016-07-01 00:00:00pages
599-605issue
1eissn
1791-2997issn
1791-3004journal_volume
14pub_type
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