ArticleScientific reports2017
Profiling of the transcriptional response to all-trans retinoic acid in breast cancer cells reveals RARE-independent mechanisms of gene expression.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- The antileukemic activity of decitabine upon PML/RARA-negative AML blasts is supported by all-trans retinoic acid: in vitro and in vivo evidence for cooperation.Blood cancer journal · 2022Trial
- Retinoic Acid and Long Noncoding RNAs Crosstalk: Implications for Neuronal Differentiation and Diseases.Molecular neurobiology · 2026Review
- Selective inhibition of ALDH1A3 impedes breast cancer growth and metastasis by blocking ALDH1A3-driven transcriptional programs.iScience · 2026Article
- Vitamins A and D and Their Combinations for Breast and Colorectal Cancers: Analysis of the Clinical, Epidemiological, Preclinical and Transcriptomic Data.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
- Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet.Oxidative medicine and cellular longevity · 2025Article
- ALDH1A3 is the switch that determines the balance of ALDHOncogene · 2024Article
- Anti-tumor activity of all-trans retinoic acid in gastric-cancer: gene-networks and molecular mechanisms.Journal of experimental & clinical cancer research : CR · 2023Article
- Review
- Mechanisms underlying the changes in acetaldehyde dehydrogenase 1 in cholangiocarcinoma.Journal of Cancer · 2023Review
- Article
- Metabolite profiling reveals a connection between aldehyde dehydrogenase 1A3 and GABA metabolism in breast cancer metastasis.Metabolomics : Official journal of the Metabolomic Society · 2022Article
- Multilayer omics analysis reveals a non-classical retinoic acid signaling axis that regulates hematopoietic stem cell identity.Cell stem cell · 2022Article
- Aldehyde dehydrogenase 1A1 and 1A3 isoforms - mechanism of activation and regulation in cancer.Cellular signalling · 2021Review
- Non-Coding RNAs in Retinoic Acid as Differentiation and Disease Drivers.Non-coding RNA · 2021Review
- A ligand-independent fast function of RARα promotes exit from metabolic quiescence upon T cell activation and controls T cell differentiation.Mucosal immunology · 2021Article
- ATPR triggers acute myeloid leukaemia cells differentiation and cycle arrest via the RARα/LDHB/ERK-glycolysis signalling axis.Journal of cellular and molecular medicine · 2020Article
- Retinoic Acids in the Treatment of Most Lethal Solid Cancers.Journal of clinical medicine · 2020Review
- ALDH1A3-regulated long non-coding RNA NRAD1 is a potential novel target for triple-negative breast tumors and cancer stem cells.Cell death and differentiation · 2020Article
- 2'-Hydroxyflavanone induced changes in the proteomic profile of breast cancer cells.Journal of proteomics · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Retinoids, derivatives of vitamin A, are key physiological molecules with regulatory effects on cell differentiation, proliferation and apoptosis. As a result, they are of interest for cancer therapy. Specifically, models of breast cancer have varied responses to manipulations of retinoid signaling. This study characterizes the transcriptional response of MDA-MB-231 and MDA-MB-468 breast cancer cells to retinaldehyde dehydrogenase 1A3 (ALDH1A3) and all-trans retinoic acid (atRA). We demonstrate limited overlap between ALDH1A3-induced gene expression and atRA-induced gene expression in both cell lines, suggesting that the function of ALDH1A3 in breast cancer progression extends beyond its role as a retinaldehyde dehydrogenase. Our data reveals divergent transcriptional responses to atRA, which are largely independent of genomic retinoic acid response elements (RAREs) and consistent with the opposing responses of MDA-MB-231 and MDA-MB-468 to in vivo atRA treatment. We identify transcription factors associated with each gene set. Manipulation of the IRF1 transcription factor demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). This study provides a paradigm for complex responses of breast cancer models to atRA treatment, and illustrates the need to characterize RARE-independent responses to atRA in a variety of models.
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