ArticleOncogene2002
Her2/neu induces all-trans retinoic acid (ATRA) resistance in breast cancer cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 72 citations in OpenAlex.
- An Efficient Suppression of EGFR and B-Raf mRNA Overexpression in the Lung of Benzo[a]pyrene-induced mice by Cationic Lipo-ATRA Nanoformulation.Recent patents on nanotechnology · 2025Article
- Review
- DNA Methylation Predicts the Response of Triple-Negative Breast Cancers to All-Trans Retinoic Acid.Cancers · 2018Article
- Synergistic antitumor activity by combining trastuzumab with retinoic acid in HER2 positive human breast cancer cells.Oncotarget · 2018Article
- Why Differentiation Therapy Sometimes Fails: Molecular Mechanisms of Resistance to Retinoids.International journal of molecular sciences · 2018Review
- ATRA increases iodine uptake and inhibits the proliferation and invasiveness of human anaplastic thyroid carcinoma SW1736 cells: Involvement of β-catenin phosphorylation inhibition.Oncology letters · 2017Article
- ω-3 free fatty acids and all-trans retinoic acid synergistically induce growth inhibition of three subtypes of breast cancer cell lines.Scientific reports · 2017Article
- Cellular retinoid binding-proteins, CRBP, CRABP, FABP5: Effects on retinoid metabolism, function and related diseases.Pharmacology & therapeutics · 2017Review
- Phosphoproteome and Transcriptome of RA-Responsive and RA-Resistant Breast Cancer Cell Lines.PloS one · 2016Article
- Differences and homologies of chromosomal alterations within and between breast cancer cell lines: a clustering analysis.Molecular cytogenetics · 2014Article
- Vitamin A and retinoid signaling: genomic and nongenomic effects.Journal of lipid research · 2013Review
- Transcriptome profiling and genome-wide DNA binding define the differential role of fenretinide and all-trans RA in regulating the death and survival of human hepatocellular carcinoma Huh7 cells.Biochemical pharmacology · 2013Article
- A retinoic acid receptor RARα pool present in membrane lipid rafts forms complexes with G protein αQ to activate p38MAPK.Oncogene · 2012Article
- Cullin 3 mediates SRC-3 ubiquitination and degradation to control the retinoic acid response.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Primary trastuzumab resistance: new tricks for an old drug.Annals of the New York Academy of Sciences · 2010Article
- Trastuzumab Sensitizes Ovarian Cancer Cells to EGFR-targeted Therapeutics.Journal of ovarian research · 2010Article
- Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations.Breast cancer research : BCR · 2010Article
- Dynamic and combinatorial control of gene expression by nuclear retinoic acid receptors (RARs).Nuclear receptor signaling · 2009Review
- A coordinated phosphorylation cascade initiated by p38MAPK/MSK1 directs RARalpha to target promoters.The EMBO journal · 2009Article
- Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We observed that all-trans retinoic acid (ATRA) inhibited the growth of MCF-7 breast cancer cells, but not those transfected with HER2/NEU or its transactivating ligand HEREGULIN. This suggests that Her2/neu causes breast cancer cells to be resistant to the growth inhibitory effects of ATRA. To confirm this observation, MDA-MB-453 and BT-474 cells, which have high levels of Her2/neu and are resistant to ATRA, were incubated with the trastuzumab (Herceptin) antibody so that we could determine whether inhibition of the expression and function of Her2/neu would resensitize these cells to ATRA. Indeed, we found that MDA-MB-453 and BT-474 cells treated with trastuzumab were growth inhibitory by ATRA. We then determined whether Her2/neu uses Grb2 and Akt proteins to induce ATRA resistance. Liposome-incorporated Grb2 antisense oligonucleotides (L-Grb2) and a dominant negative (DN) AKT mutant were used to down-regulate Grb2 expression and inhibit Akt activity, respectively. When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Our results indicate that Her2/neu utilizes Grb2 and Akt proteins to induce ATRA resistance in breast cancer cells. ATRA sensitivity was also correlated with RARalpha protein levels since higher RARalpha protein levels were observed in cells in which the Her2/neu pathway was inhibited.
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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.