ArticleBritish journal of cancer2004
Tumour necrosis factor and PI3-kinase control oestrogen receptor alpha protein level and its transrepression function.
Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 29 citations in OpenAlex.
- The IL6-like Cytokine Family: Role and Biomarker Potential in Breast Cancer.Journal of personalized medicine · 2021Review
- Intrinsic and Extrinsic Factors Governing the Transcriptional Regulation of ESR1.Hormones & cancer · 2020Review
- Effect of macrophages on breast cancer cell proliferation, and on expression of hormone receptors, uPAR and HER-2.International journal of oncology · 2017Article
- APOBEC3B-Mediated Cytidine Deamination Is Required for Estrogen Receptor Action in Breast Cancer.Cell reports · 2015Article
- Oncostatin-M promotes phenotypic changes associated with mesenchymal and stem cell-like differentiation in breast cancer.Oncogene · 2014Article
- Interplay between estrogen receptor and AKT in estradiol-induced alternative splicing.BMC medical genomics · 2013Article
- Control of EVI-1 oncogene expression in metastatic breast cancer cells through microRNA miR-22.Oncogene · 2011Article
- Inositol polyphosphate 4-phosphatase II regulates PI3K/Akt signaling and is lost in human basal-like breast cancers.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Expression of a phosphorylated p130(Cas) substrate domain attenuates the phosphatidylinositol 3-kinase/Akt survival pathway in tamoxifen resistant breast cancer cells.Journal of cellular biochemistry · 2009Article
- Review
- Article
- Extreme growth factor signalling can promote oestrogen receptor-alpha loss: therapeutic implications in breast cancer.Breast cancer research : BCR · 2004Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Oestrogen receptor alpha (ERalpha) is an oestrogen-activated transcription factor, which regulates proliferation and differentiation of mammary epithelial cells by activating or repressing gene expression. ERalpha is a critical prognostic indicator and a therapeutic target for breast cancer. Patients with tumours that express higher level of ERalpha have better prognosis than patients with tumours that are ERalpha negative or express lower level of ERalpha. Better prognosis in ERalpha-positive patients is believed to be due to repression of proinvasive gene expression by ERalpha. Oestrogen receptor alpha represses gene expression by transrepressing the activity of the transcription factors such as nuclear factor-kappaB or by inducing the expression of transcriptional suppressors such as MTA3. In this report, we show that ERalpha transrepresses the expression of the proinvasive gene interleukin 6 (IL-6) in ERalpha-negative MDA-MB-231 breast cancer cells stably overexpressing ERalpha. Using these cells as well as ERalpha-positive MCF-7 and ZR-75-1 cells, we show that tumour necrosis factor alpha (TNFalpha) and the phosphatidylinositol-3-kinase (PI3-kinase) modulate transrepression function of ERalpha by reducing its stability. From these results, we propose that TNFalpha expression or PI3-kinase activation lead to reduced levels of ERalpha protein in cancer cells and corresponding loss of transrepression function and acquisition of an invasive phenotype.
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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.