Inhibitory effect of a Ras homologue member I on pancreatic cancer and its modulation on epithelium growth factor receptor-Ras-Raf-mitogen-activated protein kinase/extracellular regulated protein kinase/1/2 pathway.
- Author:
Jia LU
1
;
Jia-ming QIAN
;
Hong YANG
;
Jing-nan LI
;
Feng-ji XU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Proliferation; Epidermal Growth Factor; metabolism; Humans; Mitogen-Activated Protein Kinase 3; metabolism; Pancreatic Neoplasms; metabolism; pathology; Receptor, Epidermal Growth Factor; metabolism; Signal Transduction; Transfection; Tumor Cells, Cultured; ras Proteins; metabolism; rho GTP-Binding Proteins; genetics
- From: Acta Academiae Medicinae Sinicae 2012;34(3):197-201
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the regulation of epithelium growth factor receptor (EGFR), pan-Ras, and extracellular regulated protein kinase (ERK) with both a ras homologue member I (ARHI) suppression and epithelium growth factor (EGF) stimulation.
METHODSAfter identification and implication, the constructed plasmid pIRES2-EGFP-ARHI was transfected into Panc-1. The untransfected cell was also explored as controls. The growth curve was drawn to indicate the proliferation effect of ARHI. EGFR-ELISA was performed to investigate the expression of EGFR. Western blot analysis was used to investigate the expression of protein MAPK/ERK1/2, pan-Ras in Panc-1.
RESULTSThe proliferation rate of Panc-1 was inhibited by ARHI compared with both empty plasmid and untransfected cell. The amount of EGFR was parallel in both transfected and untransfected cell but affected by EGF stimulation. The amount of pan-Ras was decreased after ARHI transfection. The optimum concentration of EGF effect on P-ERK was 50 ng/ml.
CONCLUSIONBoth ARHI and EGF play roles in the EGF-EGFR-Ras-Raf-MAPK/ERK1/2 pathway.
