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NLRP1 and NLRP3 inflammasomes as a new approach to skin carcinogenesis.


ABSTRACT: Inflammasomes are key innate immune system receptors that detect pathogenic endo- and exogenous stressors like microorganisms or ultraviolet radiation (UVR) which activate the highly proinflammatory cytokines interleukin-1? and interleukin-18. Inflammasomes are not only involved in inflammation, but also in carcinogenesis and tumor progression. Due to the dynamic increase in non-melanoma skin cancers (NMSC), it has become necessary to determine how UVR, which plays a key role in NMSC development, can regulate the structure and function of inflammasomes. In the present study, the regulatory mechanisms of NOD-Like Receptor Family Pyrin Domain Containing 1 and 3 inflammasome activation as well as an effective inflammasome-mediated immune response after UVR exposition are discussed. The differences and similarities between these molecular complexes that monitor cellular health, inflammation, and skin carcinogenesis are also highlighted. Despite numerous scientific data, more studies are still required to better understand the biology of inflammasomes in skin cancer development and to explore their therapeutic potential.

SUBMITTER: Ciazynska M 

PROVIDER: S-EPMC7039172 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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NLRP1 and NLRP3 inflammasomes as a new approach to skin carcinogenesis.

Ciążyńska Magdalena M   Bednarski Igor A IA   Wódz Karolina K   Narbutt Joanna J   Lesiak Aleksandra A  

Oncology letters 20200109 3


Inflammasomes are key innate immune system receptors that detect pathogenic endo- and exogenous stressors like microorganisms or ultraviolet radiation (UVR) which activate the highly proinflammatory cytokines interleukin-1β and interleukin-18. Inflammasomes are not only involved in inflammation, but also in carcinogenesis and tumor progression. Due to the dynamic increase in non-melanoma skin cancers (NMSC), it has become necessary to determine how UVR, which plays a key role in NMSC development  ...[more]

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