Responses of pancreatic cancer cells to stimulations by nerve growth factor and the role of Trk-A expression.
- Author:
Dong-Mei DIAO
1
;
Yong-Chun SONG
;
Ni HOU
;
Hai-Fei XU
;
Jian-Guang WANG
;
Cheng-Xue DANG
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Cell Movement; drug effects; Cell Proliferation; drug effects; Humans; Neoplasm Invasiveness; Nerve Growth Factor; pharmacology; Pancreatic Neoplasms; metabolism; pathology; Receptor, trkA; genetics; metabolism
- From: Journal of Southern Medical University 2012;32(3):296-300
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the responses of different pancreatic cancer cells to stimulations by nerve growth factor (NGF) and explore the role of Trk-A in such responses.
METHODSFive pancreatic cancer cell lines (MIA-PaCa-2, PANC-1, SW-1990, AsPC-1, and BxPC-3) were exposed to different concentrations of NGF (0, 4, 20, 100, and 500 ng/ml). MTT and Matrigel invasion method were used to observe the changes in the cell proliferation and invasion ability. Trk-A expression in these cells was detected by PCR and Western blotting, and the relations of Trk-A expression to the cell proliferative and invasive abilities following NGF treatment were analyzed.
RESULTSNGF at 100 ng/ml most obviously stimulated the cell proliferation, and PANC-1 cells showed the highest while AsPC-1 cells showed the least sensitivity to 100 ng/ml NGF stimulation. Matrigel invasion test showed that NGF enhanced the invasiveness of PANC-1 and MIA-PaCa-2 cells but produced only limited effect on AsPC-1 cells; the effect of NGF was completely inhibited by the Trk-A inhibitor CEP701. The expression levels of Trk-A mRNA and protein were the highest in PANC-1 cells and the lowest in AsPC-1 cells.
CONCLUSIONNGF can enhance the proliferation and invasiveness of pancreatic cancer cells, and this effect is possibly mediated by Trk-A protein.