ArticleHuman molecular genetics2010
Loss of IGF2 imprinting is associated with abrogation of long-range intrachromosomal interactions in human cancer cells.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 54 citations in OpenAlex.
- Widespread allele-specific topological domains in the human genome are not confined to imprinted gene clusters.Genome biology · 2023Article
- Melatonin and cancer suppression: insights into its effects on DNA methylation.Cellular & molecular biology letters · 2022Article
- Profound alterations of the chromatin architecture at chromosome 11p15.5 in cells from Beckwith-Wiedemann and Silver-Russell syndromes patients.Scientific reports · 2020Article
- IMAGE: high-powered detection of genetic effects on DNA methylation using integrated methylation QTL mapping and allele-specific analysis.Genome biology · 2019Article
- A Loss of Epigenetic Control Can Promote Cell Death through Reversing the Balance of Pathways in a Signaling Network.Molecular cell · 2018Article
- DNA methylation in human diseases.Genes & diseases · 2018Review
- Impairment of IGF2 gene expression in prostate cancer is triggered by epigenetic dysregulation of IGF2-DMR0 and its interaction with KLF4.Cell communication and signaling : CCS · 2017Article
- CRISPR Cas9-guided chromatin immunoprecipitation identifies miR483 as an epigenetic modulator of IGF2 imprinting in tumors.Oncotarget · 2017Article
- Loss of insulin-like growth factor II imprinting is a hallmark associated with enhanced chemo/radiotherapy resistance in cancer stem cells.Oncotarget · 2016Article
- IGF2-derived miR-483 mediated oncofunction by suppressing DLC-1 and associated with colorectal cancer.Oncotarget · 2016Article
- Increased In Vitro Osteopotential in SHED Associated with Higher IGF2 Expression When Compared with hASCs.Stem cell reviews and reports · 2015Article
- Identifying multi-locus chromatin contacts in human cells using tethered multiple 3C.BMC genomics · 2015Article
- Promoter histone H3K27 methylation in the control of IGF2 imprinting in human tumor cell lines.Human molecular genetics · 2014Article
- Induced DNA demethylation can reshape chromatin topology at the IGF2-H19 locus.Nucleic acids research · 2013Article
- Article
- Promoter cross-talk via a shared enhancer explains paternally biased expression of Nctc1 at the Igf2/H19/Nctc1 imprinted locus.Nucleic acids research · 2013Article
- Analysis of long-range chromatin interactions using Chromosome Conformation Capture.Methods (San Diego, Calif.) · 2012Article
- Chromatin structure, epigenetic mechanisms and long-range interactions in the human insulin locus.Diabetes, obesity & metabolism · 2012Review
- Cancer control and prevention by nutrition and epigenetic approaches.Antioxidants & redox signaling · 2012Review
- Targeting epigenetic mediators of gene expression in thoracic malignancies.Biochimica et biophysica acta · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Nuclear architecture and chromatin geography are important factors in the regulation of gene expression, as these components may play a vital epigenetic role both in normal physiology as well as in the initiation and progression of malignancies. Using a modification of the chromosome conformation capture (3C) technique, we examined long-range chromatin interactions of the imprinted human IGF2 gene. We demonstrate that numerous intrachromosomal interactions occur along both parental alleles in normal tissues, where the IGF2 is paternally expressed, as well as in normal liver where gene expression is biallelic. Long-range and allele-specific interactions occur between the IGF2/H19 imprinting control region-1 (ICR1) and ICR2, a region which regulates an imprinted gene cluster nearly a megabase distant from IGF2. Loss of genomic imprinting is a common epigenetic event in cancer, and long-range interactions have not been examined in malignant cells. In cancer cell lines in which IGF2 imprinting is maintained (MOI), essentially all of the 3C interactions seen in normal cells were preserved. However, in cells in which IGF2 imprinting was lost (LOI), nearly all of the long-range chromatin interactions involving IGF2 were abrogated. A three-dimensional computer model depicts the physical interactions between the IGF2 promoter and ICR1 in MOI cells, while the model of LOI lung cancer cells is flattened with few long-range interactions. This dramatic change in the three-dimension configuration of the chromatin at the IGF2 locus in LOI cancer cells suggests that the loss of imprinting may lead to a variety of changes in gene expression in addition to changes in IGF2 transcription.
Indexed as
Identifiers
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.