PMID- 33277869
OWN - NLM
STAT- MEDLINE
DCOM- 20210820
LR  - 20210820
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 25
IP  - 5
DP  - 2020 Sep-Oct
TI  - Effects of aspirin on pancreatic cancer cells PANC-1 and its potential molecular 
      mechanism.
PG  - 2449-2455
AB  - PURPOSE: To explore the effects of aspirin on the proliferation and apoptosis of 
      human pancreatic cancer cells and its potential molecular mechanism. METHODS: 
      This study included patients with pancreatic cancer who were divided into 
      experimental group and control group. The cell proliferation ability was detected 
      via cell counting kit-8 (CCK-8) assay and colony forming ability via colony 
      formation assay. In addition, changes in proteins in the phosphatidyl 
      inositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin 
      (mTOR) pathway were assessed using Western blotting, and rescue experiment was 
      conducted to investigate whether aspirin can affect cell proliferation by 
      inhibiting the PI3K/Akt/mTOR signaling pathway. RESULTS: The results of CCK-8 
      assay showed that the proliferation rate of PANC-1 cells was decreased in a time- 
      and dose-dependent manner after they were treated with aspirin at different 
      concentrations. Colony formation assay confirmed that cell colony forming ability 
      was significantly reduced with the increase in aspirin treatment concentration 
      (p<0.05). Besides, the apoptosis rate and the number of cells in the experimental 
      group were higher and larger than those in the control group (p<0.05). According 
      to Western blotting results, the protein expressions of PI3K, phosphorylated 
      (p)-Akt and p-mTOR were decreased after aspirin treatment. Rescue experimental 
      results manifested that insulin-like growth factor 1 (IGF-1) supplementation 
      remarkably elevated the expressions of PI3K, p-Akt and p-mTOR compared with 
      phosphate-buffered saline (PBS) supplementation. It was found in CCK-8 assay that 
      IGF-1 supplementation markedly reversed the inhibition of aspirin on the 
      proliferation of PANC-1 cells in comparison with PBS supplementation. 
      CONCLUSIONS: Aspirin inhibits the proliferation and promotes the apoptosis of 
      pancreatic cancer cells by inactivating the PI3K/Akt/mTOR signaling pathway.
FAU - Lin, Shengping
AU  - Lin S
AD  - Department of Emergency, Sir Run Run Shaw Hospital, Zhejiang University School of 
      Medicine, Hangzhou, China.
FAU - Pan, Yun
AU  - Pan Y
FAU - Xu, Chenglei
AU  - Xu C
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  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Apoptosis
MH  - Aspirin/pharmacology/*therapeutic use
MH  - Cell Proliferation
MH  - Humans
MH  - Pancreatic Neoplasms/*drug therapy
EDAT- 2020/12/06 06:00
MHDA- 2021/08/21 06:00
CRDT- 2020/12/05 05:35
PHST- 2020/12/05 05:35 [entrez]
PHST- 2020/12/06 06:00 [pubmed]
PHST- 2021/08/21 06:00 [medline]
PST - ppublish
SO  - J BUON. 2020 Sep-Oct;25(5):2449-2455.