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J BUON. 2019 Mar-Apr;24(2):739-745.

A study on the mechanism of rapamycin mediating the sensitivity of pancreatic cancer cells to cisplatin through PI3K/AKT/mTOR signaling pathway.

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1
Department of General Surgery, Second Hospital of Tianjin Medical University, Tianjin, China.

Abstract

PURPOSE:

To study the mechanism of rapamycin mediating the sensitivity of pancreatic cancer cells to cisplatin through phosphatidylinositol 3-kinase (PI3K)/serine-threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling pathway in vitro.

METHODS:

SW1990 cells were cultured in vitro and treated with rapamycin, cisplatin, and rapamycin combined with cisplatin, respectively, with dimethyl sulphoxide (DMSO) as the control. Cell Counting Kit-8 (CCK-8) and flow cytometry were adopted for determination of cell proliferation and apoptosis levels, respectively. The changes in PI3K/AKT/mTOR signal transmission were detected via Western blotting and reverse transcription polymerase chain reaction (RT-PCR), respectively.

RESULTS:

1: Compared with those in DMSO blank control group, the proliferation level of pancreatic cancer cells was markedly decreased and the cell apoptosis rate was remarkably increased in simple drug group (p<0.05). 2: The combined administration group had markedly decreased proliferation level and remarkably increased cell apoptosis rate of human pancreatic cancer cells, compared with those in the rapamycin alone group or cisplatin alone group (p<0.05). 3: Rapamycin combined with cisplatin could inhibit the expressions of PI3K, AKT and phosphorylated mTOR (p-mTOR) in pancreatic cancer cells (p<0.05).

CONCLUSION:

Rapamycin combined with cisplatin can alter the PI3K/AKT/mTOR signal transduction pathway which leads to markedly increased cell apoptosis rate, indicating that rapamycin can mediate the sensitivity of pancreatic cancer cells to cisplatin.

PMID:
31128031
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