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논문 기본 정보

자료유형
학술저널
저자정보
Wang Chen (China Pharmaceutical University) Ni Jiaping (China Pharmaceutical University) Zhai Dongqing (China Pharmaceutical University) Xu Yanchao (Nanjing Drum Tower Hospital Clinical College of Jiangsu University) Wu Zijie (China Pharmaceutical University) Chen Yuyuan (China Pharmaceutical University) Liu Ning (Ningxia Medical University) Du Juan (Ningxia Medical University) Shen Yumeng (China Pharmaceutical University) Liu Guilai (China Pharmaceutical University) Yang Yong (China Pharmaceutical University) You Linjun (China Pharmaceutical University) Hu Weiwei (China Pharmaceutical University)
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine Vol.56
발행연도
2024.5
수록면
1,150 - 1,163 (14page)
DOI
10.1038/s12276-024-01223-0

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Hepatocellular carcinoma (HCC) is associated with a poor prognosis. Our previous study demonstrated that Pleomorphic adenoma gene like-2 (PLAGL2) was a potential therapeutic target in HCC. However, the mechanisms that lead to the upregulation of PLAGL2 in HCC remain unclear. The present study revealed that stress-induced epinephrine increased the expression of PLAGL2, thereby promoting the progression of HCC. Furthermore, PLAGL2 knockdown inhibited epinephrine-induced HCC development. Mechanistically, epinephrine upregulated ubiquitin-specific protease 10 (USP10) to stabilize PLAGL2 via the adrenergic β-receptor-2-c-Myc (ADRB2-c-Myc) axis. Furthermore, PLAGL2 acted as a transcriptional regulator of USP10, forming a signaling loop. Taken together, these results reveal that stress-induced epinephrine activates the PLAGL2-USP10 signaling loop to enhance HCC progression. Furthermore, PLAGL2 plays a crucial role in psychological stress-mediated promotion of HCC progression.

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