p21Cip/WAF1 activation is an important factor for the ERK pathway dependent anti-proliferation of colorectal cancer cells
Experimental & Molecular Medicine
;
: 557-562, 2004.
Article
in English
| WPRIM
| ID: wpr-145924
ABSTRACT
p21Cip/WAF1, an important regulator of cell proliferation, is induced by both p53- and extracellular signal regulated kinase (ERK) pathways. The induction of p21Cip/WAF1 occurs by prolonged activation of the ERKs caused by extracellular stimuli, such as zinc. However, not all the cells appeared to respond to ERK pathway dependent p21Cip/WAF1 induction. Here we investigated the cause of such difference using colorectal cancer cells. p21Cip/WAF1 induction and concomitant reduction of bromodeoxyuridine (BrdU) incorporation were observed by zinc treatment within HT-29 and DLD-1. However, HCT-116 cells with high endogenous p21Cip/WAF1 levels did not show any additional increment of p21Cip/WAF1 levels by zinc treatment and did maintain high BrdU incorporation level. The p21Cip/WAF1 induction by zinc depended upon prolonged activation of extracellular signal regulated kinase (ERK) was not observed in HCT-116 cells. The percentage of BrdU positive cells was 50% higher in p21Cip/WAF1 -/- HCT-116 cells compared to p21Cip/WAF1 +/+ HCT- 116 cells, and no cells induced p21Cip/WAF1 incorporated BrdU in its nucleus, yet confirming the importance of p21Cip/WAF1 induction in anti- proliferation. These results again support that p21Cip/WAF1 induction is a determinant in the regulation of colonic proliferation by the ERK pathway.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Zinc
/
Flavonoids
/
Bromodeoxyuridine
/
Colorectal Neoplasms
/
Signal Transduction
/
Cell Cycle Proteins
/
Cell Line, Tumor
/
Extracellular Signal-Regulated MAP Kinases
/
Protein Kinase Inhibitors
/
Cell Proliferation
Limits:
Humans
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2004
Type:
Article
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