ArticleOncogene2000
Reversal of an antiestrogen-mediated cell cycle arrest of MCF-7 cells by viral tumor antigens requires the retinoblastoma protein-binding domain.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- RB1-deficient prostate tumor growth and metastasis are vulnerable to ferroptosis induction via the E2F/ACSL4 axis.The Journal of clinical investigation · 2023Article
- Case report: 16-yr life history and genomic evolution of an ERCold Spring Harbor molecular case studies · 2020Article
- Non-canonical functions of the RB protein in cancer.Nature reviews. Cancer · 2018Review
- Minireview: The Link Between ERα Corepressors and Histone Deacetylases in Tamoxifen Resistance in Breast Cancer.Molecular endocrinology (Baltimore, Md.) · 2016Review
- RB1 dual role in proliferation and apoptosis: cell fate control and implications for cancer therapy.Oncotarget · 2015Review
- The other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axis.Cell cycle (Georgetown, Tex.) · 2014Review
- The p53-estrogen receptor loop in cancer.Current molecular medicine · 2013Review
- Expression ratio of CCND1 to CDKN2A mRNA predicts RB1 status of cultured cancer cell lines and clinical tumor samples.Molecular cancer · 2011Article
- Targeting the RB-pathway in cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- Tailoring to RB: tumour suppressor status and therapeutic response.Nature reviews. Cancer · 2008Review
- G1 arrest and expression of cyclin-dependent kinase inhibitors in tamoxifen-treated MCF-7 human breast cancer cells.Human cell · 2008Article
- Regulation of hormonal therapy resistance by cell cycle machinery.Gene therapy & molecular biology · 2008Article
- Functional ablation of pRb activates Cdk2 and causes antiestrogen resistance in human breast cancer cells.PloS one · 2007Article
- Involvement of G1/S cyclins in estrogen-independent proliferation of estrogen receptor-positive breast cancer cells.Oncogene · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Proliferation of MCF-7 cells is estrogen dependent and antiestrogen sensitive. In the absence of estrogens or presence of antiestrogens MCF-7 cells arrest in the G1 phase of the cell cycle, and this arrest is associated with an accumulation of the active, hypophosphorylated form of the retinoblastoma protein (pRb). Because active pRb negatively regulates passage from G1 to S phase, this suggests that pRb is a crucial target of estrogen action, and that its inactivation might lead to antiestrogen resistance. We tested this hypothesis by expressing viral tumor antigens (T antigens), which bind and inactivate pRb, in MCF-7 cells, and determining the effects on cell proliferation in the presence of antiestrogens. The results of these experiments demonstrate that T antigen expression confers antiestrogen resistance to MCF-7 cells. Using a panel of mutant T antigens, we further demonstrate that the pRb-binding, but not the p53 binding domain is required to confer antiestrogen resistance. Thus, pRb is an important target of estrogen action, and its inactivation can contribute to the development of antiestrogen resistance.
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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.