Apple Polyphenols Affect Protein Kinase C Activity and the Onset of Apoptosis in Human Colon Carcinoma Cells

2007 ◽  
Vol 55 (13) ◽  
pp. 4999-5006 ◽  
Author(s):  
Melanie Kern ◽  
Gudrun Pahlke ◽  
Kamal Kumar Balavenkatraman ◽  
Frank D. Böhmer ◽  
Doris Marko
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Kinase C ◽  
Human Colon Carcinoma ◽  
Protein Kinase C Activity

Protein kinase C and casein kinase II activities in two human colon carcinoma cell lines, HT-29 and CaCo-2: Possible correlation with differentiation

1990 ◽  
Vol 10 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Ewa Rydell ◽  
Karl-Eric Magnusson ◽  
Anita Sjö ◽  
Krister Axelsson
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Colon Carcinoma ◽  
Carcinoma Cell ◽  
Human Colon ◽  
Human Colon Carcinoma Cell ◽  
Carcinoma Cell Lines ◽  
Kinase C ◽  
Human Colon Carcinoma ◽  
Ht 29

Protein kinase C (PK-C) and casein kinase II (CK-II) activities were studied in two human colon carcinoma cell lines (HT-29 and CaCO-2) undergoing differentiation in vitro resulting, in small-intestine-like cells. CaCo-2 cells, when grown under standard conditions, appear to undergo spontaneous differentiation. In these cells PK-C and CK-II activities were determined on day 5, 10 and 15. No significant differences in activities were seen either in PK-C or CK-II activity. HT-29 cells, when grown in glucose-free medium can be stimulated to undergo differentiation which is completed within 20 days. PK-C and CK-II activities were determined after 5, 10, 15, 20 and 25 days, respectively. PK-C activity rose from 7.9±3.5 pmole32P/mg protein/min at day 5 to 37.5±14.8 pmole32P/mg protein/min at day 20. After 25 days the activity was reduced to 20.0±7.8 pmole32P/mg protein/min. CK-II activity did not change significantly during day 5 to 20, but on day 25 there was a significant decrease in CK-II activity from 94.9±6.4 pmole32P/mg protein/min (day 20) to 62.6±3.9 pmole32P/mg protein/min (day 25) p=0.003. The results in this study indicate a role for PK-C and CK-II in cell growth and differentiation.

scholarly journals Expression of protein kinase C ?1 confers resistance to TNF?- and paclitaxel-induced apoptosis in HT-29 colon carcinoma cells

2001 ◽  
Vol 93 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Patrizia Cesaro ◽  
Elisabetta Raiteri ◽  
Marina D�moz ◽  
Roberta Castino ◽  
Francesco M. Baccino ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Colon Carcinoma ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Kinase C ◽  
Induced Apoptosis ◽  
Ht 29

scholarly journals Tumorigenesis Suppressor Pdcd4 Down-Regulates Mitogen-Activated Protein Kinase Kinase Kinase Kinase 1 Expression To Suppress Colon Carcinoma Cell Invasion

2006 ◽  
Vol 26 (4) ◽  
pp. 1297-1306 ◽  
Author(s):  
Hsin-Sheng Yang ◽  
Connie P. Matthews ◽  
Timothy Clair ◽  
Qing Wang ◽  
Alyson R. Baker ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Colon Carcinoma ◽  
Ectopic Expression ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Mitogen Activated Protein Kinase ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Mitogen Activated Protein ◽  
Protein Kinase Kinase

ABSTRACT Programmed cell death 4 (Pdcd4) suppresses neoplastic transformation by inhibiting the activation of c-Jun and consequently AP-1-dependent transcription. We report that Pdcd4 blocks c-Jun activation by inhibiting the expression of mitogen-activated protein kinase kinase kinase kinase 1 (MAP4K1)/hematopoietic progenitor kinase 1, a kinase upstream of Jun N-terminal kinase (JNK). cDNA microarray analysis of Pdcd4-overexpressing RKO human colon carcinoma cells revealed MAP4K1 as the sole target of Pdcd4 on the JNK activation pathway. Cotransfection of a MAP4K1 promoter-reporter with Pdcd4 demonstrated inhibition of transcription from the MAP4K1 promoter. Ectopic expression of Pdcd4 in metastatic RKO cells suppressed invasion. MAP4K1 activity is functionally significant in invasion, as overexpression of a dominant negative MAP4K1 (dnMAP4K1) mutant in RKO cells inhibited not only c-Jun activation but also invasion. Overexpression of a MAP4K1 cDNA in Pdcd4-transfected cells rescued the kinase activity of JNK. Thus, Pdcd4 suppresses tumor progression in human colon carcinoma cells by the novel mechanism of down-regulating MAP4K1 transcription, with consequent inhibition of c-Jun activation and AP-1-dependent transcription.

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