ArticleBiology2022
The CpG Island-Binding Protein SAMD1 Contributes to an Unfavorable Gene Signature in HepG2 Hepatocellular Carcinoma Cells.
Article in Biology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The SAMD1 transcription factor coordinates hematopoietic lineage differentiation and H3K4 methylation status.Blood advances · 2025Article
- Cooperation of a polymerizing SAM domain and an intrinsically disordered region enables full SAMD1 function on chromatin.Nucleic acids research · 2025Article
- SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma.PLoS biology · 2024Article
- Roles of Interferon Regulatory Factor 1 in Tumor Progression and Regression: Two Sides of a Coin.International journal of molecular sciences · 2024Review
- SAMD1 attenuates antiphospholipid syndrome-induced pregnancy complications.Immunity, inflammation and disease · 2023Article
- Hydrogen sulfide suppresses HMedical oncology (Northwood, London, England) · 2023Article
- Investigation of SAMD1 ablation in mice.Scientific reports · 2023Article
- The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA binding winged helix domain.Nucleic acids research · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The unmethylated CpG island-binding protein SAMD1 is upregulated in many human cancer types, but its cancer-related role has not yet been investigated. Here, we used the hepatocellular carcinoma cell line HepG2 as a cancer model and investigated the cellular and transcriptional roles of SAMD1 using ChIP-Seq and RNA-Seq. SAMD1 targets several thousand gene promoters, where it acts predominantly as a transcriptional repressor. HepG2 cells with SAMD1 deletion showed slightly reduced proliferation, but strongly impaired clonogenicity. This phenotype was accompanied by the decreased expression of pro-proliferative genes, including MYC target genes. Consistently, we observed a decrease in the active H3K4me2 histone mark at most promoters, irrespective of SAMD1 binding. Conversely, we noticed an increase in interferon response pathways and a gain of H3K4me2 at a subset of enhancers that were enriched for IFN-stimulated response elements (ISREs). We identified key transcription factor genes, such as
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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 OpenQuestion graph.