Abstract：
:Sustained proliferation of cancer cells requires telomerase to maintain telomeres that regulate chromosomal stability and cellular mitosis. Expression of human telomerase reverse transcriptase (hTERT) catalytic subunit, which modulates telomerase activity, is regulated at both the transcriptional level and via phosphorylation by Akt kinase. Moreover, nuclear localization of hTERT is required to promote elongation of telomere sequences. In this study, we show for the first time that hTERT protein interacts directly with nuclear factor (NF)-kappaB p65 in MM.1S cells. Importantly, tumor necrosis factor alpha (TNFalpha) modulates telomerase activity by inducing translocation from the cytoplasm to the nucleus of hTERT protein bound to NF-kappaB p65. Conversely, a specific IkappaB kinase (IKK) inhibitor PS-1145, and a specific NF-kappaB nuclear translocation inhibitor SN-50, both block TNFalpha-induced hTERT nuclear translocation. These studies suggest that NF-kappaB p65 plays a pivotal role in regulating telomerase by modulating its nuclear translocation.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Akiyama M,Hideshima T,Hayashi T,Tai YT,Mitsiades CS,Mitsiades N,Chauhan D,Richardson P,Munshi NC,Anderson KCsubject
Has Abstractpub_date
2003-01-01 00:00:00pages
18-21issue
1eissn
0008-5472issn
1538-7445journal_volume
63pub_type
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