Department of Cancer Biology, Biochemistry, College of Medicine, Univeristy of Toledo, Health Science Campus, 3035 Arlington Ave., Toledo, OH 43614, USA
TAK1 variant D activated by siRNAs of specific sequences leads to down stream activation of p38 MAPK and JNK but not NFkB pathway. In human lung cancer cell line NCI-H460 the activation of these pathway cause cell cycle arrest and apoptosis. It suggests that TAK1 D may be a new and promising therapeutic target for the treatment of non-small cell lung cancer.
Telomeres are essential elements at the ends of chromosomes that contribute to chromosomal stability. The length of the telomere is maintained by the telomerase holoenzyme, which contains the reverse transcriptase hTERT as a major enzymatic subunit. The activity of telomerase is absent in most normal human cells because of the downregulation of the hTERT transcript resulting in the shortening of telomeres after each replicative cycle. However, in immortalized cells and cancer cells, the telomere lengths are maintained through an increase in hTERT expression. TAK1 can repress the transcription of hTERT in A549 human lung adenocarcinoma cell line and this repression is caused by recruitment of HDAC to the hTERT promoter.
Hui Hui Tang ; Kam C Yeung
MAP3K7 (mitogen-activated protein kinase kinase kinase 7)
Atlas Genet Cytogenet Oncol Haematol. 2009-03-01
Online version: http://atlasgeneticsoncology.org/gene/454/map3k7id454ch6q15