Journal
BREAST CANCER RESEARCH AND TREATMENT
Volume 137, Issue 2, Pages 329-336Publisher
SPRINGER
DOI: 10.1007/s10549-012-2351-7
Keywords
Transcription factors; Feedback loop; Cell signaling; Drug resistance; DNA damage response
Categories
Funding
- NIH [R01-CA102289]
- Ocala Royal Dames for Cancer Research
- Florida Department of Health
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Owing to numerous pro-survival target genes, aberrant activation of the NF-kappa B transcription factor is associated with a drug-resistant phenotype and aggressive breast tumor behavior. Transglutaminase 2 (TG2), a ubiquitously expressed protein cross-linking enzyme, activates NF-kappa B through a non-conventional mechanism that disables the I kappa B alpha inhibitor. Our group has recently documented that the TG2 gene (termed TGM2) is a direct transcriptional target of NF-kappa B. These developments uncover a novel self-reinforcing molecular feedback loop where TG2 activates NF-kappa B and, in turn, NF-kappa B directly upregulates the transcription of TGM2. This manuscript reviews the literature that supports the existence of the TG2/NF-kappa B signaling loop, the nature of the signal transduction that activates this loop, and the phenotypic consequences stemming from the aberrant activation of this novel signaling mechanism in breast cancer.
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