ArticleMolecular cancer2013
Id4 deficiency attenuates prostate development and promotes PIN-like lesions by regulating androgen receptor activity and expression of NKX3.1 and PTEN.
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- EZH2 dependent H3K27me3 is involved in epigenetic silencing of ID4 in prostate cancer.Oncotarget · 2014Pooled it
- The Critical Role of Inhibitor of Differentiation 4 in Breast Cancer: From Mammary Gland Development to Tumor Progression.Cancer medicine · 2025Review
- ELK3-ID4 axis governs the metastatic features of triple negative breast cancer.Oncology research · 2023Article
- The Current State of Chromatin Immunoprecipitation (ChIP) from FFPE Tissues.International journal of molecular sciences · 2022Review
- Targeted Disruption of theInternational journal of molecular sciences · 2021Article
- Inhibitor of Differentiation 4 (ID4) represses mammary myoepithelial differentiation via inhibition of HEB.iScience · 2021Article
- The helix-loop-helix transcriptional regulator Id4 is required for terminal differentiation of luminal epithelial cells in the prostate.Oncoscience · 2021Article
- TIP5 primes prostate luminal cells for the oncogenic transformation mediated byProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Epigenomic profiling of archived FFPE tissues by enhanced PAT-ChIP (EPAT-ChIP) technology.Clinical epigenetics · 2018Article
- Epigenetic regulation of ID4 in breast cancer: tumor suppressor or oncogene?Clinical epigenetics · 2018Article
- Inactivation of ID4 promotes a CRPC phenotype with constitutive AR activation through FKBP52.Molecular oncology · 2017Article
- Intra-tumoral delivery of functional ID4 protein via PCL/maltodextrin nano-particle inhibits prostate cancer growth.Oncotarget · 2016Article
- ID4 promotes AR expression and blocks tumorigenicity of PC3 prostate cancer cells.Biochemical and biophysical research communications · 2016Article
- Basic helix loop helix (bHLH) transcription factor 3 (TCF3, E2A) is regulated by androgens in prostate cancer cells.American journal of cancer research · 2015Article
- Inhibitor of differentiation 4 (ID4): From development to cancer.Biochimica et biophysica acta · 2015Review
- Prostate cancer epigenome.Methods in molecular biology (Clifton, N.J.) · 2015Review
- Inhibitor of differentiation 4 (ID4) inactivation promotes de novo steroidogenesis and castration-resistant prostate cancer.Molecular endocrinology (Baltimore, Md.) · 2014Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundInhibitor of differentiation 4 (Id4), a member of the helix-loop-helix family of transcriptional regulators has emerged as a tumor suppressor in prostate cancer. Id4 is expressed in the normal prostate where its expression is also regulated by androgens. In this study we investigated the effect of loss of Id4 (Id4-/-) on adult prostate morphology.
methodsHistological analysis was performed on prostates from 6-8 weeks old Id4-/-, Id4+/- and Id4+/+ mice. Expression of Id1, Sox9, Myc, androgen receptor, Akt, p-Akt, Pten and Nkx3.1 was investigated by immunohistochemistry. Androgen receptor binding on NKX3.1 promoter was studied by chromatin immuno-precipitation. Id4 was either over-expressed or silenced in prostate cancer cell lines DU145 and LNCaP respectively followed by analysis of PTEN, NKX3.1 and Sox9 expression.
resultsId4-/- mice had smaller prostates with fewer tubules, smaller tubule diameters and subtle mPIN like lesions. Levels of androgen receptor were similar between wild type and Id4-/- prostate. Decreased NKX3.1 expression was in part due to decreased androgen receptor binding on NKX3.1 promoter in Id4-/- mice. The increase in the expression of Myc, Sox9, Id1, Ki67 and decrease in the expression of PTEN, Akt and phospho-AKT was associated with subtle mPIN like lesions in Id4-/- prostates. Finally, prostate cancer cell line models in which Id4 was either silenced or over-expressed confirmed that Id4 regulates NKX3.1, Sox9 and PTEN.
conclusionsOur results suggest that loss of Id4 attenuates normal prostate development and promotes hyperplasia/dysplasia with subtle mPIN like lesions characterized by gain of Myc and Id1 and loss of Nkx3.1 and Pten expression. One of the mechanisms by which Id4 may regulate normal prostate development is through regulating androgen receptor binding to respective response elements such as those on NKX3.1 promoter. In spite of these complex alterations, large neoplastic lesions in Id4-/- prostates were not observed suggesting the possibility of mechanisms/pathways such as loss of Akt that could restrain the formation of significant pre-cancerous lesions.
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