ArticleBMC cancer2017
Loss of DIP2C in RKO cells stimulates changes in DNA methylation and epithelial-mesenchymal transition.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Integration of methylome and transcriptome reveals age-associated signatures of stage-specific dynamics and regulatory remodeling in dogs.GeroScience · 2026Article
- Serum DIP2C protein concentration in human colorectal cancer among Yemeni patients.Frontiers in oncology · 2026Article
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- Transcriptomic profiling ofComputational and structural biotechnology journal · 2024Article
- An epigenome-wide study of selenium status and DNA methylation in the Strong Heart Study.Environment international · 2024Article
- Novel liquid biopsy CNV biomarkers in malignant melanoma.Scientific reports · 2024Article
- De novo variants predicting haploinsufficiency for DIP2C are associated with expressive speech delay.American journal of medical genetics. Part A · 2024Article
- Genetic architecture of childhood speech disorder: a review.Molecular psychiatry · 2024Review
- Chicken Hypothalamic and Ovarian DNA Methylome Alteration in Response to Forced Molting.Animals : an open access journal from MDPI · 2023Article
- Cancer-derived exosomal miR-375 targets DIP2C and promotes osteoblastic metastasis and prostate cancer progression by regulating the Wnt signaling pathway.Cancer gene therapy · 2023Article
- Establishing a human bone marrow single cell reference atlas to study ageing and diseases.Frontiers in immunology · 2023Article
- Article
- DNA methylome in visceral adipose tissue can discriminate patients with and without colorectal cancer.Epigenetics · 2022Article
- Arsenic exposure and human blood DNA methylation and hydroxymethylation profiles in two diverse populations from Bangladesh and Spain.Environmental research · 2022Article
- DNA Methylation in Babies Born to Nonsmoking Mothers Exposed to Secondhand Smoke during Pregnancy: An Epigenome-Wide Association Study.Environmental health perspectives · 2021Article
- Multi-omics analysis to identify susceptibility genes for colorectal cancer.Human molecular genetics · 2021Article
- Case Report: Clinical Description of a Patient Carrying a 12.48 Mb Microdeletion Involving the 10p13-15.3 Region.Frontiers in pediatrics · 2021Article
- Genome-Wide Association Studies Reveal Susceptibility Loci for Noninfectious Claw Lesions in Holstein Dairy Cattle.Frontiers in genetics · 2021Article
- Peri-natal growth retardation rate and fat mass accumulation in mice lacking Dip2A is dependent on the dietary composition.Transgenic research · 2020Article
- Targeted Disruption of Mouse Dip2B Leads to Abnormal Lung Development and Prenatal Lethality.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe disco-interacting protein 2 homolog C (DIP2C) gene is an uncharacterized gene found mutated in a subset of breast and lung cancers. To understand the role of DIP2C in tumour development we studied the gene in human cancer cells.
methodsWe engineered human DIP2C knockout cells by genome editing in cancer cells. The growth properties of the engineered cells were characterised and transcriptome and methylation analyses were carried out to identify pathways deregulated by inactivation of DIP2C. Effects on cell death pathways and epithelial-mesenchymal transition traits were studied based on the results from expression profiling.
resultsKnockout of DIP2C in RKO cells resulted in cell enlargement and growth retardation. Expression profiling revealed 780 genes for which the expression level was affected by the loss of DIP2C, including the tumour-suppressor encoding CDKN2A gene, the epithelial-mesenchymal transition (EMT) regulator-encoding ZEB1, and CD44 and CD24 that encode breast cancer stem cell markers. Analysis of DNA methylation showed more than 30,000 sites affected by differential methylation, the majority of which were hypomethylated following loss of DIP2C. Changes in DNA methylation at promoter regions were strongly correlated to changes in gene expression, and genes involved with EMT and cell death were enriched among the differentially regulated genes. The DIP2C knockout cells had higher wound closing capacity and showed an increase in the proportion of cells positive for cellular senescence markers.
conclusionsLoss of DIP2C triggers substantial DNA methylation and gene expression changes, cellular senescence and epithelial-mesenchymal transition in cancer cells.
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