ArticleCell cycle (Georgetown, Tex.)2022
SAMHD1, positively regulated by KLF4, suppresses the proliferation of gastric cancer cells through MAPK p38 signaling pathway.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization.Oncogene · 2025Article
- Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells.Open life sciences · 2025Article
- KLF4: a multifunctional nexus connecting tumor progression and immune regulation.Frontiers in immunology · 2025Review
- Palmitoyl-carnitine Regulates Lung Development by Promoting Pulmonary Mesenchyme Proliferation.Research (Washington, D.C.) · 2025Article
- Identification of anti-gastric cancer effects and molecular mechanisms of resveratrol: From network pharmacology and bioinformatics to experimental validation.World journal of gastrointestinal oncology · 2024Article
- Article
- SAMHD1 restricts the deoxyguanosine triphosphate pool contributing to telomere stability in telomerase-positive cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SAMHD1 was reported to be related with the development of tumors, while its function in gastric cancer (GC) has not been elucidated yet. Here, we investigated the role and mechanism of SAMHD1 in regulating the proliferation of GC, as well as the mechanism of its expression regulation. Our results revealed that SAMHD1 was downregulated in GC tissues and cell lines, which was correlated with tumor size, depth of invasion and TNM stage. Overexpression of SAMHD1 inhibited the proliferation, clone formation, DNA synthesis and cell cycle progression, while knockdown of SAMHD1 promoted the proliferation of GC cells in vitro and vivo. Meanwhile, SAMHD1 inhibited the activation of MAPK p38 signaling pathway. Moreover, SB203580, as a MAPK p38 inhibitor, could reverse the proliferation and activation of MAPK p38 signaling pathway caused by knockdown of SAMHD1 in GC cells. Additionally, transcription factor Krüppel-like factor 4 (KLF4) bound to the core promoter of SAMHD1, increasing its transcriptional expression in GC cells. In conclusion, SAMHD1 suppressed the proliferation of GC through negatively regulating the activation of MAPK p38 signaling pathway and was upregulated by KLF4 in GC cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.