These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: (‑)‑Epigallocatechin‑3‑gallate induces apoptosis in human pancreatic cancer cells via PTEN.
    Author: Liu S, Xu ZL, Sun L, Liu Y, Li CC, Li HM, Zhang W, Li CJ, Qin W.
    Journal: Mol Med Rep; 2016 Jul; 14(1):599-605. PubMed ID: 27176210.
    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.
    [Abstract] [Full Text] [Related] [New Search]