ArticleBritish journal of cancer2014
Delayed triggering of oestrogen induced apoptosis that contrasts with rapid paclitaxel-induced breast cancer cell death.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Advances in nano drug delivery systems for enhanced efficacy of emodin in cancer therapy.International journal of pharmaceutics: X · 2025Review
- PERK, Beyond an Unfolded Protein Response Sensor in Estrogen-Induced Apoptosis in Endocrine-Resistant Breast Cancer.Molecular cancer research : MCR · 2022Review
- Estrogen Receptor Complex to Trigger or Delay Estrogen-Induced Apoptosis in Long-Term Estrogen Deprived Breast Cancer.Frontiers in endocrinology · 2022Review
- The effect of paclitaxel on apoptosis, autophagy and mitotic catastrophe in AGS cells.Scientific reports · 2021Article
- Turning scientific serendipity into discoveries in breast cancer research and treatment: a tale of PhD students and a 50-year roaming tamoxifen team.Breast cancer research and treatment · 2021Review
- Microbiome-host co-oscillation patterns in remodeling of colonic homeostasis during adaptation to a high-grain diet in a sheep model.Animal microbiome · 2020Article
- Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein.Molecular cancer research : MCR · 2019Article
- Modulation of nuclear factor-kappa B activation by the endoplasmic reticulum stress sensor PERK to mediate estrogen-induced apoptosis in breast cancer cells.Cell death discovery · 2018Article
- The molecular, cellular and clinical consequences of targeting the estrogen receptor following estrogen deprivation therapy.Molecular and cellular endocrinology · 2015Review
- Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells.Molecular cancer research : MCR · 2015Article
- The new biology of estrogen-induced apoptosis applied to treat and prevent breast cancer.Endocrine-related cancer · 2015Review
- Article
- Avoiding the bad and enhancing the good of soy supplements in breast cancer.Journal of the National Cancer Institute · 2014Article
- Differences in the rate of oestrogen-induced apoptosis in breast cancer by oestradiol and the triphenylethylene bisphenol.British journal of pharmacology · 2014Article
- Anastrozole-Induced Tumor Lysis Syndrome in Breast Cancer: A Case Report of a Rare Critical Care Emergency.Case reports in oncologyArticle
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOestrogen (E2) induces apoptosis in long-term E2-deprived MCF7 cells (MCF7:5C). Taxanes have been used extensively in the treatment of early and advanced breast cancer. We have interrogated the sequence of events that involve the apoptotic signalling pathway induced by E2 in comparison with paclitaxel.
methodsDNA quantification and cell cycle analysis were used to assess proliferation of cancer cells. Apoptosis was evaluated using annexin V and DNA staining methods. Regulation of apoptotic genes was determined by performing PCR-based arrays and RT-PCR.
resultsE2-induced apoptosis is a delayed process, whereas paclitaxel immediately inhibits the growth and induces death of MCF7:5C cells. The cellular commitment for E2-triggered apoptosis occur after 24 h. Activation of the intrinsic pathway was observed by 36 h of E2 treatment with subsequent induction of the extrinsic apoptotic pathway by 48 h. Paclitaxel exclusively activated extramitochondrial apoptotic genes and caused rapid G2/M blockade by 12 h of treatment. By contrast, E2 causes an initial proliferation with elevated S phase of cell cycles followed by apoptosis of the MCF7:5C cells. Most importantly, we are the first to document that E2-induced apoptosis can be reversed after 24 h treatment.
conclusionsThese data indicate that E2-induced apoptosis involves a novel, multidynamic process that is distinctly different from that of a classic cytotoxic chemotherapeutic drug used in breast cancer.
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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.