Effects of paxillin on HCT-8 human colorectal cancer cells.

Abstract

BACKGROUND/AIMS:

The aim of this study was to investigate the effects of paxillin on proliferation, migration, invasion, adhesion and apoptosis of HCT-8 human colorectal cancer cells in vitro.

METHODOLOGY:

siRNA plasmids, overexpression wild-type plasmids and overexpression mutant plasmids were generated and transfected into HCT-8 cells. The expression of paxillin mRNA and protein was analyzed, and cell proliferation and adhesion were measured. Flow cytometry was used for cell sorting and detection of cell apoptosis. The invasive ability of HCT-8 cells was also observed.

RESULTS:

The proliferation, migration and invasive capacity of the HCT-8 cells transfected with siRNA paxillin plasmids were inhibited. Overexpression of wild-type paxillin plasmids promoted cell proliferation and also enhanced migration, invasive capacity and metastasis of the cancer cells. Overexpression of mutant paxillin plasmids inactivated the function of phosphorylation, inhibited cell migration and invasion capacity, but cell adhesion and proliferation had no significant difference compared with the normal group.

CONCLUSIONS:

These findings suggest that paxillin may play an essential role in the progression of colorectal cancer and RNAi targeting of paxillin may be a potential therapeutic strategy for the treatment of colorectal cancer.

• Authors: Qin Jun, Wang Zhiwei, Ma Lilin, Ke Jing, Ni Qichao
• Journal: Hepato-gastroenterology (Hepatogastroenterology) 2011 Nov-Dec Vol. 58 Issue 112 Pg. 1951-5 ISSN: 0172-6390 [Print] Greece
• PMID: 21940355 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• PXN protein, human
• Paxillin
• RNA, Small Interfering

Topics

• Apoptosis
• Cell Line, Tumor
• Cell Movement
• Colorectal Neoplasms (etiology, pathology, therapy)
• Disease Progression
• Gene Expression Regulation
• Humans
• Neoplasm Invasiveness
• Paxillin (antagonists & inhibitors, genetics, physiology)
• Plasmids
• RNA, Small Interfering (genetics)