ArticleScientific reports2015
Mechanisms of Gefitinib-mediated reversal of tamoxifen resistance in MCF-7 breast cancer cells by inducing ERα re-expression.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Non-coding RNA-mediated mechanisms underlying tamoxifen resistance in breast cancer.Discover oncology · 2026Review
- Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.Nature communications · 2025Article
- MAPK signaling mediates tamoxifen resistance in estrogen receptor-positive breast cancer.Molecular and cellular biochemistry · 2025Review
- Cancer Cells Show Higher Sensitivity to Melatonin-Tamoxifen Drug Conjugates than to Combination of Melatonin and Tamoxifen.ACS omega · 2024Article
- Potential of covalently linked tamoxifen hybrids for cancer treatment: recent update.RSC medicinal chemistry · 2024Review
- Receptor tyrosine kinases in breast cancer treatment: unraveling the potential.American journal of cancer research · 2024Review
- Development of Gefitinib-Loaded Solid Lipid Nanoparticles for the Treatment of Breast Cancer: Physicochemical Evaluation, Stability, and Anticancer Activity in Breast Cancer (MCF-7) Cells.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Therapeutic significance of molecular hybrids for breast cancer research and treatment.RSC medicinal chemistry · 2023Review
- GDNF-RET signaling and EGR1 form a positive feedback loop that promotes tamoxifen resistance via cyclin D1.BMC cancer · 2023Article
- Anticancer Drug Conjugates Incorporating Estrogen Receptor Ligands.Pharmaceutics · 2022Review
- Pharmacophore-based virtual screening approaches to identify novel molecular candidates against EGFR through comprehensive computational approaches andFrontiers in pharmacology · 2022Article
- Blockade of CDK7 Reverses Endocrine Therapy Resistance in Breast Cancer.International journal of molecular sciences · 2020Article
- 4,5-Diaryl 3(Molecules (Basel, Switzerland) · 2019Article
- Encircling the regions of the pharmacogenomic landscape that determine drug response.Genome medicine · 2019Article
- Receptor tyrosine kinases (RTKs) in breast cancer: signaling, therapeutic implications and challenges.Molecular cancer · 2018Review
- Protein Kinase Targets in Breast Cancer.International journal of molecular sciences · 2017Review
- Oestrogen receptor negativity in breast cancer: a cause or consequence?Bioscience reports · 2016Review
- Acupoint Thread Embedding Combined With Wenshen Bugu Decoction for the Treatment of Aromatase Inhibitor-Associated Musculoskeletal Symptom Among Postmenopausal Breast Cancer Patients: Study Protocol of a Randomized Controlled Trial.Integrative cancer therapiesArticle
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptor (ER)-positive breast cancer patients may turn ER-negative and develop acquired drug resistance, which compromises the efficacy of endocrine therapy. By investigating the phenomenon that gefitinib can re-sensitise tamoxifen (TAM)-resistant MCF-7 breast cancer cells (MCF-7/TAM) to TAM, the present study verified that gefitinib could reverse the acquired drug resistance in endocrine therapy and further explored the underlying mechanism.ERα-negative MCF-7/TAM cells were established. Upon treating the cells with gefitinib, the mRNA and protein levels of ERα and ERβ, as well as the expression of molecules involved in the MAPK pathway, were examined using the RT-PCR and immunocytochemistry. The RT-PCR results showed that the mRNA levels of ERα and ERβ in MCF-7/TAM cells were up-regulated following gefitinib treatment; specifically, ERα was re-expressed, and ERβ expression was up-regulated. The expression of molecules involved in the MAPK pathway, including RAS, MEK1/2, and p-ERK1/2, in MCF-7/TAM cells was significantly up-regulated, compared with MCF-7 cells. After the gefitinib treatment, the expression levels of MEK1/2 and p-ERK1/2 were significantly down-regulated. ERα loss is the primary cause for TAM resistance. Gefitinib reverses TAM resistance primarily by up-regulating the ERα mRNA level and inducing the re-expression of ERα. The MAPK pathway plays a key role in ERα re-expression.
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