Research Papers:

Hypoxia primes human normal prostate epithelial cells and cancer cell lines for the NLRP3 and AIM2 inflammasome activation

Ravichandran Panchanathan, Hongzhu Liu and Divaker Choubey _

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Oncotarget. 2016; 7:28183-28194. https://doi.org/10.18632/oncotarget.8594

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Ravichandran Panchanathan1,2, Hongzhu Liu1,2, Divaker Choubey1,2

1Cincinnati VA Medical Center, Cincinnati, OH 45220, USA

2Department of Environmental Health, University of Cincinnati, Cincinnati, OH 45267, USA

Correspondence to:

Divaker Choubey, email: [email protected]

Keywords: hypoxia, prostate, inflammasome, inflammation, cancer

Received: December 15, 2015     Accepted: March 28, 2016     Published: April 5, 2016


The molecular mechanisms by which hypoxia contributes to prostatic chronic inflammation (PCI) remain largely unknown. Because hypoxia stimulates the transcriptional activity of NF-κB, which “primes” cells for inflammasome activation by inducing the expression of NLRP3 or AIM2 receptor and pro-IL-1β, we investigated whether hypoxia could activate the NLRP3 and AIM2 inflammasome in human normal prostate epithelial cells (PrECs) and cancer cell lines. Here we report that hypoxia (1% O2) treatment of PrECs, prostate cell lines, and a macrophage cell line (THP-1) increased the levels of NLRP3, AIM2, and pro-IL-1β. Further, hypoxia in cells potentiated activation of the NLRP3 and AIM2 inflammasome activity. Notably, hypoxia “primed” cells for NLRP3 and AIM2 inflammasome activation through stimulation of the NF-κB activity. Our observations support the idea that hypoxia in human prostatic tumors contributes to PCI, in part, by priming cells for the activation of NLRP3 and AIM2 inflammasome.

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