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Stat2 stability regulation: an intersection between immunity and carcinogenesis

Experimental & Molecular Medicine 2020년 52권 9호 p.24 ~ 24
Lee Cheol-Jung, 안현정, 조은서, Kang Han-Chang, 이주영, 이혜숙, Cho Yong-Yeon,
소속 상세정보
 ( Lee Cheol-Jung ) - Catholic University College of Pharmacy
안현정 ( An Hyun-Jung ) - Catholic University College of Pharmacy
조은서 ( Cho Eun-Suh ) - Catholic University College of Pharmacy
 ( Kang Han-Chang ) - Catholic University College of Pharmacy
이주영 ( Lee Joo-Young ) - Catholic University College of Pharmacy
이혜숙 ( Lee Hye-Suk ) - Catholic University College of Pharmacy
 ( Cho Yong-Yeon ) - Catholic University College of Pharmacy

Abstract


Signal transducer and activator of transcription (STAT2) is a member of the STAT family that plays an essential role in immune responses to extracellular and intracellular stimuli, including inflammatory reactions, invasion of foreign materials, and cancer initiation. Although the majority of STAT2 studies in the last few decades have focused on interferon (IFN)-α/β (IFNα/β) signaling pathway-mediated host defense against viral infections, recent studies have revealed that STAT2 also plays an important role in human cancer development. Notably, strategic research on STAT2 function has provided evidence that transient regulatory activity by homo- or heterodimerization induces its nuclear localization where it to forms a ternary IFN-stimulated gene factor 3 (ISGF3) complex, which is composed of STAT1 and/or STAT2 and IFN regulatory factor 9 (IEF9). The molecular mechanisms of ISGF3-mediated ISG gene expression provide the basic foundation for the regulation of STAT2 protein activity but not protein quality control. Recently, previously unknown molecular mechanisms of STAT2-mediated cell proliferation via STAT2 protein quality control were elucidated. In this review, we briefly summarize the role of STAT2 in immune responses and carcinogenesis with respect to the molecular mechanisms of STAT2 stability regulation via the proteasomal degradation pathway.

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