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MiR-146-NF-κB pathway is a key axis in the regulation of FOXP3-deficient prostate cancers

 

FOXP3, a member of the forkhad-box/winged-helix transcription factor family, has been reported as a T cell transcription factor, as well as a tumor suppressor gene in prostate cancer. However, the underlying mechanisms of FOXP3 functions as a tumor suppressor gene remains elusive. Liu et al. from University of Alabama at Birmingham reveal FOXP3-microRNA-146(miR-146)-NF-κB axis as a critical signaling pathway in regulating the survival of prostate cancer cells both in vitro and in vivo. The article was published in Cancer Research, recently.

 

FOXP3 strongly induced the expression of miR-146a/b, led to the inhibition of IRAK1 and TRAF6 in transcriptional level in prostate cancer cells lines. On the other hand, Deletion of Foxp3 in a mouse prostate tissue-specific manner significantly reduced miR-146a as well as increase NF-κB signaling. Researchers observed prostatic intraepithelial neoplasia lesions in miR-146a mutant mice and Foxp3 mutant mice. This symptom was attenuated using NF-κB inhibitor bortezomib in Foxp3 mutant mice, indicating NF-κB plays as a upregulator in the survival of prostate epithelial cells. These findings suggest targeting the miR-146-NF-κB axis may be a promising therapeutic strategy for FOXP3-deficient prostate cancers.

 

Reference:
Cancer Res. 2015 Feb 23. pii: canres.2109.2014.

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Proteasome