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논문 기본 정보

자료유형
학술저널
저자정보
Ke Shanjia (The First Affiliated Hospital of Harbin Medical University) Lu Shounan (The First Affiliated Hospital of Harbin Medical University) Xu Yanan (Zhejiang University School of Medicine) Bai Miaoyu (The First Affiliated Hospital of Harbin Medical University) Yu Hongjun (The First Affiliated Hospital of Harbin Medical University) Yin Bing (The First Affiliated Hospital of Harbin Medical University) Wang Chaoqun (the Second Affiliated Hospital of Army Medical University) Feng Zhigang (The First Affiliated Hospital of Harbin Medical University) Li Zihao (The First Affiliated Hospital of Harbin Medical University) Huang Jingjing (The First Affiliated Hospital of Harbin Medical University) Li Xinglong (The First Affiliated Hospital of Harbin Medical University) Qian Baolin (The First Affiliated Hospital of Harbin Medical University) Hua Yongliang (The First Affiliated Hospital of Harbin Medical University) Fu Yao (The First Affiliated Hospital of Harbin Medical University) Sun Bei (The First Affiliated Hospital of Harbin Medical University) Wu Yaohua (The First Affiliated Hospital of Harbin Medical University) Ma Yong (The First Affiliated Hospital of Harbin Medical University)
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine Vol.56
발행연도
2024.6
수록면
1 - 14 (14page)
DOI
10.1038/s12276-024-01244-9

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Hepatocellular carcinoma (HCC) is one of the most common fatal cancers worldwide, and the identification of novel treatment targets and prognostic biomarkers is urgently needed because of its unsatisfactory prognosis. Regulator of G-protein signaling 19 (RGS19) is a multifunctional protein that regulates the progression of various cancers. However, the specific function of RGS19 in HCC remains unclear. The expression of RGS19 was determined in clinical HCC samples. Functional and molecular biology experiments involving RGS19 were performed to explore the potential mechanisms of RGS19 in HCC. The results showed that the expression of RGS19 is upregulated in HCC tissues and is significantly associated with poor prognosis in HCC patients. RGS19 promotes the proliferation and metastasis of HCC cells in vitro and in vivo. Mechanistically, RGS19, via its RGS domain, stabilizes the MYH9 protein by directly inhibiting the interaction of MYH9 with STUB1, which has been identified as an E3 ligase of MYH9. Moreover, RGS19 activates β-catenin/c-Myc signaling via MYH9, and RGS19 is also a transcriptional target gene of c-Myc. A positive feedback loop formed by RGS19, MYH9, and the β-catenin/c-Myc axis was found in HCC. In conclusion, our research revealed that competition between RGS19 and STUB1 is a critical mechanism of MYH9 regulation and that the RGS19/MYH9/β-catenin/c-Myc feedback loop may represent a promising strategy for HCC therapy.

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