IMR Press / FBE / Volume 3 / Issue 1 / DOI: 10.2741/E249

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

TNF-α mediated NF-kappaB activation is constantly extended by transglutaminase 2

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1 Cancer Cell and Molecular Biology Branch, Goyang, Gyeonggi-do 410-769, Republic of Korea
2 Genitourinary Cancer Branch, Division of Translational and Clinical Research II, National Cancer Center, Goyang, Gyeonggi-do 410-769, Republic of Korea
3 Carcinogenesis Branch, Division of Cancer Biology, Goyang, Gyeonggi-do 410-769, Republic of Korea
4 Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul 130-701, Republic of Korea

*Author to whom correspondence should be addressed.

Front. Biosci. (Elite Ed) 2011, 3(1), 341–354; https://doi.org/10.2741/E249
Published: 1 January 2011
Abstract

Increased levels of transglutaminase 2 (TGase 2) expression have been reported in many inflammatory diseases, as well as in drug resistant cancer cells. Previous reports have shown that TGase 2 is capable of inducing nuclear factor-kappaB (NF-kappaB) activation via depletion of inhibitor of kappaB (I-kappaB)α through polymerization in the absence of I-kappaBalpha kinase activation. This raises the question of whether increased expression of TGase 2 can extend NF-kappaB activation mediated by a canonical activation pathway. In the TGase 2-inducible EcR23/TG cell line, TGase 2 over-expression resulted in sustained activation of NF-κB in the presence of TNF-alpha, for up to 24 hrs, while in the absence of TGase 2 induction, NF-kappaB activity was restored to basal levels within 6 hrs of TNF-alpha treatment. In mice injected with an adenovirus vector expressing TGase 2, NF-kappaB was constitutively activated for up to 5 days, whereas Adeno/GFP-injected mice exhibited attenuated activation of NF-kappaB in response to TNF-α stress. Thus, the presence of increased levels of TGase 2 may exacerbate NF-κB activation in inflammatory states.

Keywords
transglutaminase 2
I-κBα
NF-κB
inflammation
TNF-α
Review
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