Phospholipase Cγ1 and NF-κB are required for cell-matrix adhesion of colorectal cancer cells
- VernacularTitle:磷脂酶Cγ1及NF-κB在结直肠癌细胞与基质黏附中的作用及信号转导机制
- Author:
Xiumei LI
;
Xiaochun BAI
;
Fan DENG
;
Di LU
;
Shenqiu LUO
- Publication Type:Journal Article
- Keywords:
phospholipase Cγ1;
colorectal neoplasms;
adhesion;
epidermal growth factor;
NF-κB
- From:
Academic Journal of Second Military Medical University
2005;26(5):465-470
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the function and mechanism of phospholipase Cγ1 (PLCγ1) in cell-matrix adhesion in colorectal cancer. Methods: Highly metastatic colorectal cancer cell line LoVo and lowly metastatic colorectal cancer cell line SW480 were subjected to cell-matrix adhesion assay. U73122 (a specific inhibitor of PLC) and pyrrolidine dithiocarbamate (PDTC) (an inhibitor of NF-κB) were used to study the effect of PLCγ1 and NF-κB on cell-matrix adhesion. Furthermore, Western blot and gel electrophoresis mobility shift assay (EMSA) were performed to detect the mechanism of PLCγ1 in colorectal cancer cell adhesion to matrix. Results: Inhibition of PLCγ1 or NF-κB resulted in reduction of cell-matrix adhesion in a dose-dependent manner in LoVo cells(P<0.05), but had no marked effect on SW480 cells. Western blot analysis showed that epidermal growth factor (EGF) stimulated the phosphorylation of PLCγ1 in LoVo. The results of EMSA indicated that inhibition of PLCγ1 signaling pathway also down-regulated the activity of NF-κB while EGF reversed the function. Conclusion:These data suggest that PLCγ1 plays a pivotal role in the EGF-induced cell-matrix adhesion of highly metastatic colorectal cancer cells and that NF-κB is also functional in this signaling pathway.
