ArticleOncogene2018
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Mechanistic Investigation of FBXW11-Mediated Ubiquitination and Degradation of HIC1 in Regulating IRF1 Transcription and Accelerating Acute Pancreatitis Progression.Digestive diseases and sciences · 2026Article
- Targeting the Golgi apparatus enhances PD-L1 blockade and synergizes with oxaliplatin to improve immunotherapy efficacy.The Journal of biological chemistry · 2026Article
- Structural pharmacology of Chinese medicine: technological breakthroughs in decoding multi-target synergy and precision mechanisms.Advanced biotechnology · 2026Review
- Silencer variants are key drivers of gene up-regulation in Alzheimer's disease.Science advances · 2026Article
- Cell-Free DNA Hypermethylation in Patients with Acute Pancreatitis.International journal of molecular sciences · 2025Article
- Germline pathogenic variants in HIC1 DNA binding domains are associated with familial serrated polyposis syndrome.International journal of cancer · 2025Article
- Multiomic integration reveals subtype-specific predictors of neoadjuvant treatment response in breast cancer.Science advances · 2025Article
- Targeting GSK3β and signaling pathways in breast cancer: role of individual members of miR- 23/24/27 cluster.BMC cancer · 2025Article
- DIAPH2 gene polymorphisms and laryngeal cancer risk in men.Journal of cancer research and clinical oncology · 2024Article
- Ferroptosis: a new hunter of hepatocellular carcinoma.Cell death discovery · 2024Review
- Article
- FBXW11 contributes to stem-cell-like features and liver metastasis through regulating HIC1-mediated SIRT1 transcription in colorectal cancer.Cell death & disease · 2021Article
- DIAPH2, PTPRD and HIC1 Gene Polymorphisms and Laryngeal Cancer Risk.International journal of environmental research and public health · 2021Article
- Expression of the miR-302/367 microRNA cluster is regulated by a conserved long non-coding host-gene.Scientific reports · 2021Article
- Article
- ZBTB Transcription Factors: Key Regulators of the Development, Differentiation and Effector Function of T Cells.Frontiers in immunology · 2021Review
- Trp53 and Rb1 regulate autophagy and ligand-dependent Hedgehog signaling.The Journal of clinical investigation · 2020Article
- Opposite Roles of the JMJD1A Interaction Partners MDFI and MDFIC in Colorectal Cancer.Scientific reports · 2020Article
- HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk.The Journal of clinical investigation · 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
20 authors at 6 institutions in 2 countries.
Funding
Abstract
Hypermethylated-in-Cancer 1 (Hic1) is a tumor suppressor gene frequently inactivated by epigenetic silencing and loss-of-heterozygosity in a broad range of cancers. Loss of HIC1, a sequence-specific zinc finger transcriptional repressor, results in deregulation of genes that promote a malignant phenotype in a lineage-specific manner. In particular, upregulation of the HIC1 target gene SIRT1, a histone deacetylase, can promote tumor growth by inactivating TP53. An alternate line of evidence suggests that HIC1 can promote the repair of DNA double strand breaks through an interaction with MTA1, a component of the nucleosome remodeling and deacetylase (NuRD) complex. Using a conditional knockout mouse model of tumor initiation, we now show that inactivation of Hic1 results in cell cycle arrest, premature senescence, chromosomal instability and spontaneous transformation in vitro. This phenocopies the effects of deleting Brca1, a component of the homologous recombination DNA repair pathway, in mouse embryonic fibroblasts. These effects did not appear to be mediated by deregulation of Hic1 target gene expression or loss of Tp53 function, and rather support a role for Hic1 in maintaining genome integrity during sustained replicative stress. Loss of Hic1 function also cooperated with activation of oncogenic KRas in the adult airway epithelium of mice, resulting in the formation of highly pleomorphic adenocarcinomas with a micropapillary phenotype in vivo. These results suggest that loss of Hic1 expression in the early stages of tumor formation may contribute to malignant transformation through the acquisition of chromosomal instability.
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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.