ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Nuclear Overexpression of SAMHD1 Induces M Phase Stalling in Hepatoma Cells and Suppresses HCC Progression by Interacting with the Cohesin Complex.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- SAMHD1 drives immunosuppression in non-small cell lung cancer by promoting macrophage infiltration and restricting oncolytic adenovirus replication.Journal for immunotherapy of cancer · 2026Article
- Hepatocyte SAMHD1 Deficiency Attenuates Hepatic Steatosis via Suppression of SREBP Activation in a Mouse Model of Metabolic-Associated Steatotic Liver Disease.International journal of biological sciences · 2026Article
- Regulation of eco-tropic human immunodeficiency virus type-1-infection by sterile alpha motif and histidine-aspartic domain containing protein-1 in a microglial cell line: a novel in vitro model for studying HIV infection and latency in microglia.Journal of neurovirology · 2025Article
- Nuclear Overexpression of SAMHD1 Induces M Phase Stalling in Hepatoma Cells and Suppresses HCC Progression by Interacting with the Cohesin Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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22 authors.
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Abstract
Emerging evidence suggests that the sterile alpha-motif (SAM) and histidine-aspartate (HD) domain-containing protein 1 (SAMHD1) is implicated in various cancers, including hepatocellular carcinoma (HCC). However, its precise role in tumor cells and the underlying mechanisms remain unclear. This study aimed to investigate the expression patterns, prognostic values, and functional role of SAMHD1 in HCC progression. We constructed liver tissue microarrays using tumor and paired paratumor tissue specimens from 187 patients with primary HCC. Our findings indicate that nuclear SAMHD1 protein levels are increased in tumors compared to paratumor tissues. Moreover, nuclear SAMHD1 levels decline in advanced tumor stages, with higher SAMHD1 nuclear staining correlating with favorable prognostic outcomes. Hepatocyte-specific SAMHD1 knockout mice, generated by crossing SAMHD1
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