Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.

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Tác giả: Keiichi Akahoshi, Yoshimitsu Akiyama, Kenei Furukawa, Koichiro Haruki, Megumi Hatano, Yosuke Igarashi, Toru Ikegami, Atsushi Kamachi, Keita Kodera, Atsushi Nara, Kohei Okazaki, Hiroaki Ono, Shu Shimada, Minoru Tanabe, Shinji Tanaka, Tomohiko Taniai, Yoshiaki Tanji, Shu Tsukihara, Kentaro Umemura, Shuichi Watanabe, Masahiro Yamane, Koya Yasukawa

Ngôn ngữ: eng

Ký hiệu phân loại: 553.3 Iron

Thông tin xuất bản: Netherlands : JHEP reports : innovation in hepatology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 228529

 BACKGROUND & AIMS: The inhibition of epigenetic regulators activates endogenous retrovirus (ERV) expression, which can stimulate a viral mimicry response in cancer cells. ERV elements are aberrantly expressed in hepatocellular carcinoma (HCC)
  however, the expression of ERVs regulated by histone modifications and their clinical significance in HCC remain unclear. Here, we identified specific human endogenous retrovirus (HERV) elements epigenetically suppressed by the histone methyltransferase SETDB1 in HCC. METHODS: The Cancer Genome Atlas (TCGA) dataset was analyzed to identify HERV elements based on RESULTS: TCGA analysis revealed an inverse correlation between CONCLUSIONS: The suppression of four novel HERV elements by SETDB1 serves as a prognostic marker in HCC. Activation of these SETDB1-regulated HERVs could represent a promising therapeutic strategy for HCC. IMPACT AND IMPLICATIONS: An inverse relationship between retroelements including human endogenous retrovirus (HERV) elements and
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