PMID- 23447002
OWN - NLM
STAT- MEDLINE
DCOM- 20140725
LR  - 20240102
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 7
IP  - 4
DP  - 2013 Apr
TI  - Inhibitory effect of ARHI on pancreatic cancer cells and NF-kappaB activity.
PG  - 1180-4
LID - 10.3892/mmr.2013.1342 [doi]
AB  - The aim of this study was to investigate the effect of aplasia ras homolog member 
      I (ARHI) on proliferation, apoptosis and the cell cycle in the pancreatic cancer 
      cell line PANC-1. The study also aimed to examine the effect of ARHI on the 
      activity of the nuclear factor (NF)-kappaB and to determine whether ARHI acts as a 
      tumor suppressor in the development of pancreatic cancer by inhibiting the 
      activity of NF-kappaB. A pIRES2‑EGFP‑ARHI vector, constructed by reverse transcrition 
      (RT)‑PCR, was transiently transfected into the PANC-1 cells and analyzed for the 
      expression of the ARHI protein by western blotting. A MTT assay was used to 
      quantify cell proliferation, and apoptosis was analyzed by flow cytometry. The 
      NF‑kappaB signaling pathway, specifically the pathway using the nuclear 
      phosphorylated p65 isoform, was analyzed by western blotting. Expression of the 
      ARHI protein was detected by western blotting subsequent to the PANC-1 cells 
      being transiently transfected with the pIRES2‑EGFP‑ARHI construct. Cell 
      proliferation was strongly inhibited in the PANC-1 cells transfected with 
      pIRES2‑EGFP‑ARHI. The cell cycle assays indicated an increase in the number of 
      cells at the G0/G1 phase and a decrease in the cells at the S phase, but the 
      difference was not significant (P>0.05). Time course studies also indicated a 
      marked increase in the apoptotic index following transient transfection, as well 
      as a gradual decrease in the expression of the nuclear phosphorylated p65 
      protein. ARHI acts as a tumor suppressor by downregulating the NF‑kappaB signaling 
      pathway, which results in the inhibition of cell proliferation, apoptosis and the 
      cell cycle in the pancreatic tumor PANC-1 cell line.
FAU - Hu, Yi-Qun
AU  - Hu YQ
AD  - Department of Gastroenterology, Zhongshan Hospital Affiliated to Xiamen 
      University, Xiamen, Fujian 361004, P.R. China. huyiqun0826@yahoo.com.cn
FAU - Si, Li-Juan
AU  - Si LJ
FAU - Ye, Zhen-Shi
AU  - Ye ZS
FAU - Lin, Zhen-He
AU  - Lin ZH
FAU - Zhou, Jing-Ping
AU  - Zhou JP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130226
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (DIRAS3 protein, human)
RN  - 0 (NF-kappa B)
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cell Cycle/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - NF-kappa B/biosynthesis/*genetics
MH  - Pancreatic Neoplasms/*genetics/pathology
MH  - Phosphorylation
MH  - Signal Transduction/genetics
MH  - rho GTP-Binding Proteins/*biosynthesis/genetics
EDAT- 2013/03/01 06:00
MHDA- 2014/07/26 06:00
CRDT- 2013/03/01 06:00
PHST- 2012/12/23 00:00 [received]
PHST- 2013/02/19 00:00 [accepted]
PHST- 2013/03/01 06:00 [entrez]
PHST- 2013/03/01 06:00 [pubmed]
PHST- 2014/07/26 06:00 [medline]
AID - 10.3892/mmr.2013.1342 [doi]
PST - ppublish
SO  - Mol Med Rep. 2013 Apr;7(4):1180-4. doi: 10.3892/mmr.2013.1342. Epub 2013 Feb 26.