ReviewExpert opinion on therapeutic targets2013
Deciphering HIC1 control pathways to reveal new avenues in cancer therapeutics.
Review in Expert opinion on therapeutic targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Germline pathogenic variants in HIC1 DNA binding domains are associated with familial serrated polyposis syndrome.International journal of cancer · 2025Article
- HIC1 suppresses Tumor Progression and Enhances CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Suv39h1 Regulates Phenotypic Modulation of Smooth Muscle Cells and Contributes to Vascular Injury by Repressing HIC1 Transcription.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Epigenomic Dysregulation in Youth Vapers: Implications for Disease Risk Assessment.American journal of respiratory cell and molecular biology · 2025Article
- Single-cell analysis of mesenchymal cells in permeable neural vasculature reveals novel diverse subpopulations of fibroblasts.Fluids and barriers of the CNS · 2024Article
- Dr.Nod: computational framework for discovery of regulatory non-coding drivers in tissue-matched distal regulatory elements.Nucleic acids research · 2023Article
- Synergistic activation of RARβ and RARγ nuclear receptors restores cell specialization during stem cell differentiation by hijacking RARα-controlled programs.Life science alliance · 2023Article
- Ferroptosis-related gene HIC1 in the prediction of the prognosis and immunotherapeutic efficacy with immunological activity.Frontiers in immunology · 2023Article
- Skin Aging in Long-Lived Naked Mole-Rats Is Accompanied by Increased Expression of Longevity-Associated and Tumor Suppressor Genes.The Journal of investigative dermatology · 2022Article
- Cellular taxonomy of Hic1Nature communications · 2022Article
- The Role of LncRNAs in Uveal Melanoma.Cancers · 2021Review
- Establishing a Prognostic Signature Based on Epithelial-Mesenchymal Transition-Related Genes for Endometrial Cancer Patients.Frontiers in immunology · 2021Article
- Integrated Analysis of Ferroptosis-Related Biomarker Signatures to Improve the Diagnosis and Prognosis Prediction of Ovarian Cancer.Frontiers in cell and developmental biology · 2021Article
- Article
- The transcription factor Hypermethylated in Cancer 1 (Hic1) regulates neural crest migration via interaction with Wnt signaling.Developmental biology · 2020Article
- PHF20L1 as a H3K27me2 reader coordinates with transcriptional repressors to promote breast tumorigenesis.Science advances · 2020Article
- Article
- STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment.International journal of molecular sciences · 2018Review
- Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells.Cell reports · 2018Article
- Downregulation of hypermethylated in cancer-1 byCancer cell international · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionThe tumor suppressor gene HIC1 (Hypermethylated in Cancer 1), which encodes a transcriptional repressor with multiple partners and multiple targets, is epigenetically silenced but not mutated in tumors. HIC1 has broad biological roles during normal development and is implicated in many canonical processes of cancer such as control of cell growth, cell survival upon genotoxic stress, cell migration, and motility. AREAS COVERED: The HIC1 literature herein discussed includes its discovery as a candidate tumor suppressor gene hypermethylated or deleted in many human tumors, animal models establishing it as tumor suppressor gene, its role as a sequence-specific transcriptional repressor recruiting several chromatin regulatory complexes, its cognate target genes, and its functional roles in normal tissues. Finally, this review discusses how its loss of function contributes to the early steps in tumorigenesis. EXPERT OPINION: Given HIC1's ability to direct repressive complexes to sequence-specific binding sites associated with its target genes, its loss results in specific changes in the transcriptional program of the cell. An understanding of this program through identification of HIC1's target genes and their involvement in feedback loops and cell process regulation will yield the ability to leverage this knowledge for therapeutic translation.
Indexed as
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What OpenQuestion holds
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.