Journal
NATURAL COMPOUNDS AND THEIR ROLE IN APOPTOTIC CELL SIGNALING PATHWAYS
Volume 1171, Issue -, Pages 495-500Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2009.04899.x
Keywords
genistein; ERK1/2; p38 MAPK; JNK; AKT
Categories
Funding
- Korean Government (MOEHRD) [KRF2007-313-E00380]
Ask authors/readers for more resources
Genistein, a soy-derived isoflavone, inhibits growth of tumor cells from various malignancies. Here we investigated the effect of genistein on the growth of cervical cancer cells (HeLa and CaSki) and its possible mechanism. Genistein significantly suppressed cell growth of HeLa and CaSki cells at concentrations of 20 and 60 mu mol/L, respectively, for 24 h. Western blotting analysis showed that genistein reduced phosphorylation of AKT and extracellular signal-regulated kinase (ERK)-1/2 and induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Moreover, inhibition of ERK1/2 activity enhanced cell growth inhibition by genistein, whereas inhibition of p38 MAPK activity rescued from genistein-mediated growth inhibition. Interestingly, inhibition of AKT activity recovered genistein-induced growth inhibition in CaSki cells but did not in HeLa cells. However, inhibition of JNK activity seemed to have little effect on cell growth inhibition by genistein. Taken together, these results suggest that genistein could inhibit cell growth by inhibiting ERK1/2 activity and activating p38 MAPK.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available