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논문 기본 정보

자료유형
학술저널
저자정보
Yuna Kim (Sungkyunkwan University School of Medicine) Baeki E. Kang (Sungkyunkwan University School of Medicine) Karim Gariani (Geneva University Hospitals) Joanna Gariani (Hirslanden Grangettes Clinic) Junguee Lee (Konyang University) Hyun-Jin Kim (Sungkyunkwan University School of Medicine) Chang-Woo Lee (Sungkyunkwan University School of Medicine) Kristina Schoonjans (Ecole Polytechnique Federale de Lausanne) Johan Auwerx (Ecole Polytechnique Federale de Lausanne(스위스)) Dongryeol Ryu (Sungkyunkwan University School of Medicine)
저널정보
대한생화학·분자생물학회 BMB Reports BMB Reports Vol.57 No.2
발행연도
2024.2
수록면
98 - 103 (6page)
DOI
https://doi.org/10.5483/BMBRep.2023-0187

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The mammalian sirtuin family (SIRT1–SIRT7) has shown diver se biological roles in the regulation and maintenance of ge nome stability under genotoxic stress. SIRT7, one of the leaststudied sirtuin, has been demonstrated to be a key factor forDNA damage response (DDR). However, conflicting resultshave proposed that Sirt7 is an oncogenic factor to promotetransformation in cancer cells. To address this inconsistency, weinvestigated properties of SIRT7 in hepatocellular carcinoma(HCC) regulation under DNA damage and found that loss ofhepatic Sirt7 accelerated HCC progression. Specifically, thenumber, size, and volume of hepatic tumor colonies in diethyl nitrosamine (DEN) injected Sirt7-deficient liver were markedlyenhanced. Further, levels of HCC progression markers andpro-inflammatory cytokines were significantly elevated in theabsence of hepatic Sirt7, unlike those in the control. In chro matin, SIRT7 was stabilized and colocalized to damage site byinhibiting the induction of γH2AX under DNA damage. Toge ther, our findings suggest that SIRT7 is a crucial factor for DNAdamage repair and that hepatic loss-of-Sirt7 can promote ge nomic instability and accelerate HCC development, unlike earlystudies describing that Sirt7 is an oncogenic factor.

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