PMID- 31128031
OWN - NLM
STAT- MEDLINE
DCOM- 20191121
LR  - 20220409
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 24
IP  - 2
DP  - 2019 Mar-Apr
TI  - A study on the mechanism of rapamycin mediating the sensitivity of pancreatic 
      cancer cells to cisplatin through PI3K/AKT/mTOR signaling pathway.
PG  - 739-745
AB  - 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.
FAU - Li, Baoyu
AU  - Li B
AD  - Department of General Surgery, Second Hospital of Tianjin Medical University, 
      Tianjin, China.
FAU - Yang, Jingbo
AU  - Yang J
FAU - Lu, Zenghong
AU  - Lu Z
FAU - Liu, Bin
AU  - Liu B
FAU - Liu, Fangzhou
AU  - Liu F
LA  - eng
PT  - Journal Article
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - Q20Q21Q62J (Cisplatin)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Animals
MH  - Antineoplastic Combined Chemotherapy Protocols/*pharmacology
MH  - Apoptosis/drug effects
MH  - Autophagy/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Cisplatin/*pharmacology
MH  - Drug Resistance, Neoplasm/drug effects
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Pancreatic Neoplasms/*drug therapy/genetics/pathology
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Proteins c-akt/genetics
MH  - Signal Transduction/drug effects
MH  - Sirolimus/*pharmacology
MH  - TOR Serine-Threonine Kinases/genetics
EDAT- 2019/05/28 06:00
MHDA- 2019/11/22 06:00
CRDT- 2019/05/26 06:00
PHST- 2019/05/26 06:00 [entrez]
PHST- 2019/05/28 06:00 [pubmed]
PHST- 2019/11/22 06:00 [medline]
PST - ppublish
SO  - J BUON. 2019 Mar-Apr;24(2):739-745.