2 replies to this topic

[smithx]

http://www.nature.co...ll/ncb2621.html

Telomerase directly regulates NF-κB-dependent transcription

Although elongation of telomeres is thought to be the prime function of reactivated telomerase in cancers, this activity alone does not account for all of the properties that telomerase reactivation attributes to human cancer cells. Here, we uncover a link between telomerase and NF-κB, a master regulator of inflammation. We observe that while blocking NF-κB signalling can inhibit effects of telomerase overexpression on processes relevant to transformation, increasing NF-κB activity can functionally substitute for reduced telomerase activity. Telomerase directly regulates NF-κB-dependent gene expression by binding to the NF-κB p65 subunit and recruitment to a subset of NF-κB promoters such as those of IL-6 and TNF-α, cytokines that are critical for inflammation and cancer progression. As NF-κB can transcriptionally upregulate telomerase levels, our findings suggest that a feed-forward regulation between them could be the key mechanistic basis for the coexistence of chronic inflammation and sustained telomerase activity in human cancers.

[Kevnzworld]

If I understand this correctly, this study says that there is a feedback loop of sorts between telomerase and NF-kB. The study says " We observe that while blocking NF-κB signalling can inhibit effects of telomerase overexpression on processes relevant to transformation, increasing NF-κB activity can functionally substitute for reduced telomerase activity.". I take this to mean that taking supplements that lower inflammation ( NF -kB ) inhibit telomerase over expression and subsequently cancer development. These same anti inflammatory substances have also been shown to protect telomere length. ( omega 3, curcumin etc )
So the key is protecting telomeres in ways that don't allow for telomerase " overexpression ".

[niner]

The cancer puzzle gets more convoluted as we slowly figure it out. I'm just not sure that the ramifications of overexpressed telomerase in a cancer cell will also hold in a normal cell, or even a normal cell that has telomerase expression transiently increased by the use of a drug.