ArticleMolecular biology reports2012
EGFR-mediated G1/S transition contributes to the multidrug resistance in breast cancer cells.
Article in Molecular biology reports, 2012. 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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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Combination Treatment with EGFR Inhibitor and Doxorubicin Synergistically Inhibits Proliferation of MCF-7 Cells and MDA-MB-231 Triple-Negative Breast Cancer Cells In Vitro.International journal of molecular sciences · 2024Article
- Mechanisms of chemotherapeutic resistance and the application of targeted nanoparticles for enhanced chemotherapy in colorectal cancer.Journal of nanobiotechnology · 2022Review
- Circulating syndecan-1 and glypican-4 predict 12-month survival in metastatic colorectal cancer patients.Frontiers in oncology · 2022Article
- Kinase-targeted cancer therapies: progress, challenges and future directions.Molecular cancer · 2018Review
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- MMP1 expression is activated by Slug and enhances multi-drug resistance (MDR) in breast cancer.PloS one · 2017Article
- Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer.British journal of cancer · 2014Article
- Comparison of two site-specifically (18)F-labeled affibodies for PET imaging of EGFR positive tumors.Molecular pharmaceutics · 2014Article
- Regional differences in breast cancer biomarkers in american Indian and Alaska native women.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014Article
- Combined phosphoproteomics and bioinformatics strategy in deciphering drug resistant related pathways in triple negative breast cancer.International journal of proteomics · 2014Article
- Proapoptotic and Antiproliferative Effects of Thymus caramanicus on Human Breast Cancer Cell Line (MCF-7) and Its Interaction with Anticancer Drug Vincristine.Evidence-based complementary and alternative medicine : eCAM · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the improvement of strategies against cancer therapy, the multidrug resistance (MDR)is the critical problem for successful cancer therapy. Recurrent cancers after initial treatment with chemotherapy are generally refractory to second treatments with these anticancer therapies. Therefore, it is necessary to elucidate the therapy-resistant mechanism for development of effective therapeutic modalities against tumors. Here we demonstrate a phase-specific chemotherapy resistance due to epidermal growth factor receptor (EGFR) in human breast cancer cells. Thymidine-induced G1-arrested cultures showed upregulated chemosensitivity, whereas S-phase arrested cells were more resistant to chemotherapeutic agents. Overexpression of EGFR promoted the MDR phenotypes in breast cancer cells via accelerating the G1/S phase transition, whereas depletion of EGFR exerted the opposite effects. Furthermore, CyclinD1, a protein related to cell cycle, was demonstrated to be involved in above EGFR-mediated effects since EGFR increased the expression of CyclinD1, and the specific RNA interference against CyclinD1 could primarily abolish the EGFR-induced MDR phenotypes. These data provide new insights into the mode by which MDR breast cancers evade cytoxic attacks from chemotherapeutic agents and also suggest a role for EGFR-CyclinD1 axis in this process.
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