ArticleCellular & molecular biology letters2010
Inhibitor of differentiation 1 (ID1) promotes cell survival and proliferation of prostate epithelial cells.
Article in Cellular & molecular biology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 24 citations in OpenAlex.
- ID1 and IGFBP3: roles in cellular senescence, cardiac development, angiogenesis and cancer diagnosis.Journal of translational medicine · 2023Article
- Single-cell omics traces the heterogeneity of prostate cancer cells and the tumor microenvironment.Cellular & molecular biology letters · 2023Review
- TBX3 promotes the epithelial mesenchymal transition of cervical cancer by upregulating ID1.American journal of cancer research · 2023Article
- Single-Cell RNA Sequencing Reveals Molecular Features of Heterogeneity in the Murine Retinal Pigment Epithelium.International journal of molecular sciences · 2022Article
- Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020Review
- PTBP3 Induced Inhibition of Differentiation of Gastric Cancer Cells Through Alternative Splicing of Id1.Frontiers in oncology · 2020Article
- Suppression of invasion and metastasis in aggressive salivary cancer cells through targeted inhibition of ID1 gene expression.Cancer letters · 2016Article
- The TGF-β Signaling Regulator PMEPA1 Suppresses Prostate Cancer Metastases to Bone.Cancer cell · 2015Article
- Id4 deficiency attenuates prostate development and promotes PIN-like lesions by regulating androgen receptor activity and expression of NKX3.1 and PTEN.Molecular cancer · 2013Article
- Id1 and Id3 expression is associated with increasing grade of prostate cancer: Id3 preferentially regulates CDKN1B.Cancer medicine · 2012Article
- Insulin-like growth factor I suppresses bone morphogenetic protein signaling in prostate cancer cells by activating mTOR signaling.Cancer research · 2010Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Id1 (inhibitor of differentiation 1) is a member of the bHLH protein family. Consistent with its role in promoting proliferation and inhibiting differentiation, Id1 expression is low or negligible in normal prostate epithelial cells but is high in prostate cancer. Ectopic expression of Id1 in normal prostate epithelial cells could therefore provide a model for understanding early events involved in initiation of prostate cancer. Over-expression of Id1 immortalized but did not transform ventral prostate epithelial cells (Id1-RPE). Immortalization was associated with decreased Cdkn2a, Cdkn1a, androgen receptor and increased Tert expression. Gene expression profiling over successive doublings was used to identify transcriptomic changes involved during immortalization (Tieg, Jun, alpha actin, Klf10, Id2) and in maintaining the immortalized phenotype (Igfbp3, Igfbp5, Mmp2, Tgfb3). Network analysis indicated that Id1 promotes cancer/tumor morphology, cell cycle and epithelial to mesenchymal transition by influencing AP1, tnf, tgfbeta, PdgfBB and estradiol pathways. During immortalization, the expression of majority of differentially expressed genes reduced over progressive doublings suggesting a decline in transcriptional regulatory mechanisms. The associated molecular/gene expression profile of Id1-RPE cells provides an opportunity to understand the molecular pathways associated with prostate epithelial cell survival and proliferation.
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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.