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Review
, 9 (11), 4726-4737
eCollection

IL-32θ: A Recently Identified Anti-Inflammatory Variant of IL-32 and Its Preventive Role in Various Disorders and Tumor Suppressor Activity

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Review

IL-32θ: A Recently Identified Anti-Inflammatory Variant of IL-32 and Its Preventive Role in Various Disorders and Tumor Suppressor Activity

Muhammad Babar Khawar et al. Am J Transl Res.

Abstract

Interleukin-32 theta (IL-32θ) is newly identified isoform of IL-32 which plays a vital role in inflammatory responses. Like IL-32α and IL-32β, IL-32θ isoform acts as an intracellular inflammatory modulator. It results in reduction of IL-1β production by attenuating the expression of PU.1 and inhibition of monocytes differentiation into macrophages. IL-32θ hinders TNF-α expression by inhibiting p38 MAPK and inhibitor of κB (IκB) as well. It also reserved STAT3-ZEB1 pathway leading to the inhibition of epithelial-mesenchymal transition (EMT) and stemness. Hence, it can be concluded that IL-32θ is an anti-inflammatory cytokine that can act as a tumor suppressor and can play vital role in colon cancer therapies. IL-32θ also plays a crucial role in immune system responses and cellular differentiation during disease pathogenesis. To our best knowledge this is the first ever review to condense the importance, precise mode of action in disease progression and latent remedial implications of IL-32θ in several inflammatory disorders.

Keywords: Cancer; IL-32θ; cellular differentiation; inflammation; remedial; tumor suppression.

Conflict of interest statement

None.

Figures

Figure 1
Figure 1
How IL-32θ inhibits IL-1β production: IL-32θ attenuates IL-1β production by inhibiting the PKCδ interaction to PU.1. As IL-32θ inhibits PKCδ mediated PU.1 phosphorylation it ultimately prevents IL-1β transcription and production.
Figure 2
Figure 2
Attenuation of TNF-α production by IL-32θ. PKCs promote TNF-α production through p38 MAPK and NF-κB signaling. As IL-32θ prevents nuclear translocation of NF-κB by inhibiting p38 MAPK, it ultimately prevents inflammation by inhibiting TNF-α production.
Figure 3
Figure 3
Inhibition of stemness and EMT by IL-32θ. IL-32θ interacts with STAT3 pathway to suppress ZEB1 and Bmi1 transcription and ultimately prevents stemness and EMT in colon cancer cells.

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