Customer Publication
Nuclear Overexpression of SAMHD1 Induces M Phase Stalling in Hepatoma Cells and Suppresses HCC Progression by Interacting with the Cohesin Complex
Journal: Advanced Science (2024)
Research Areas: Cancer Research
Cell Lines: HEK293T cells (GNHu44), HepG2 cells (TCHu72) and Huh7 cells (TCHu182) (hepatoma cell lines)
Summary: 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). This study aimed to investigate the expression patterns, prognostic values, and functional role of SAMHD1 in HCC progression. Data from the current study indicate that nuclear SAMHD1 protein levels are increased in tumors compared to paratumor tissues and that nuclear SAMHD1 levels decline in advanced tumor stages. In hepatoma cell lines, nuclear overexpression of SAMHD1 inhibited cell proliferation by stalling mitosis. The authors suggest that nuclear SAMHD1 plays a critical role in slowing HCC progression by regulating mitosis. Data generated using HoloMonitor shows that there is a decrease in cell proliferation and cell migration in SAMHD1-overexpressing cells.