ArticleMolecular and cellular endocrinology2012
Indole-3-carbinol disrupts estrogen receptor-alpha dependent expression of insulin-like growth factor-1 receptor and insulin receptor substrate-1 and proliferation of human breast cancer cells.
Article in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Gene Expression of Hormone Receptors and Growth Factors in Intact and Neutralized Female Dogs, Both Healthy and with Cutaneous Mast Cell Tumors.Animals : an open access journal from MDPI · 2026Article
- Protein profiling uncovers IGF-1R inhibition potential of 3-(2-furoyl)-indole scaffolds in hepatocellular carcinoma.Future medicinal chemistry · 2025Article
- Review
- Review
- Hormonal regulation of telomerase activity and hTERT expression in steroid-regulated tissues and cancer.Cancer cell international · 2022Review
- Review
- Anticancer properties of medicinal plants and their bioactive compounds against breast cancer: a review on recent investigations.Environmental science and pollution research international · 2022Review
- Review
- Extraction and Quantification of Sulforaphane and Indole-3-Carbinol from Rapeseed Tissues Using QuEChERS Coupled with UHPLC-MS/MS.Molecules (Basel, Switzerland) · 2020Article
- Protein‑ and growth‑modulatory effects of carcinoma‑associated fibroblasts on breast cancer cells: Role of interleukin‑6.International journal of oncology · 2020Article
- Mechanisms Underlying Biological Effects of Cruciferous Glucosinolate-Derived Isothiocyanates/Indoles: A Focus on Metabolic Syndrome.Frontiers in nutrition · 2020Review
- Effects of indole-3-carbinol on steroid hormone profile and tumor progression in a mice model of canine inflammatory mammarycancer.BMC cancer · 2018Article
- Pharmacophore modeling for identification of anti-IGF-1R drugs and in-vitro validation of fulvestrant as a potential inhibitor.PloS one · 2018Article
- Review
- Role of dietary bioactive natural products in estrogen receptor-positive breast cancer.Seminars in cancer biology · 2016Review
- Dietary Indoles Suppress Delayed-Type Hypersensitivity by Inducing a Switch from Proinflammatory Th17 Cells to Anti-Inflammatory Regulatory T Cells through Regulation of MicroRNA.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Sustained proliferation in cancer: Mechanisms and novel therapeutic targets.Seminars in cancer biology · 2015Review
- Essential role of the cancer stem/progenitor cell marker nucleostemin for indole-3-carbinol anti-proliferative responsiveness in human breast cancer cells.BMC biology · 2014Article
- Use of dietary phytochemicals to target inflammation, fibrosis, proliferation, and angiogenesis in uterine tissues: promising options for prevention and treatment of uterine fibroids?Molecular nutrition & food research · 2014Review
- Natural products as potential cancer therapy enhancers: A preclinical update.SAGE open medicine · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We previously established that Indole-3-Carbinol (I3C), a natural hydrolysis product of glucobrassicin in cruciferous vegetables, arrests the proliferation of estrogen-dependent human breast cancer cells and induces protein degradation of Estrogen Receptor-alpha (ERα). We demonstrate in human MCF-7 breast cancer cells that I3C ablates expression of Insulin-like Growth Factor Receptor-1 (IGF1R) and Insulin Receptor Substrate-1 (IRS1), downstream effectors of the IGF1 signaling pathway. Exogenous ERα reversed the I3C mediated loss of IGF1R and IRS1 gene expression demonstrating that down-regulation of ERα is functionally linked to I3C control of IGF1R and IRS1 expression. I3C disrupted binding of endogenous ERα, but not Sp1, to ERE-Sp1 composite elements within the IGF1R/IRS1 promoters. Exogenous ERα abrogated, and combined expression of IGF1R and IRS1 attenuated, the I3C mediated cell cycle arrest. Therefore, I3C inhibits proliferation of estrogen-sensitive breast cancer cells through disruption of ERα-mediated transcription of cell signaling components within the IGF1 cascade.
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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.