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Induction of PDCD4 tumor suppressor gene expression by RAR agonists, antiestrogen and HER-2/neu antagonist in breast cancer cells. Evidence for a role in apoptosis
Abstract
The growth of human breast tumor cells is regulated through signaling involving cell surface growth factor receptors and nuclear receptors of the steroid/thyroid/retinoid receptor gene family. Retinoic acid receptors (RARs), members of the steroid/thyroid hormone receptor gene family, are ligand-dependent transcription factors, which have in vitro and in vivo growth inhibitory activity against breast cancer cells. RAR-agonists inhibit the proliferation of many human breast cancer cell lines, particularly those whose growth is stimulated by estradiol (E2) or growth factors. Additionally, RAR-agonists and synthetic retinoids such as Ferentinide have been shown to induce apoptosis in malignant breast cells but not normal breast cells. To better define the genes involved in RAR-mediated growth inhibition of breast cancer cells, we used oligonucleotide microarray analysis to create a database of genes that are potentially regulated by RAR-agonists in breast cancer cells. We found that PDCD4 (programmed cell death 4), a tumor suppressor gene presently being evaluated as a target for chemoprevention, was induced about three-fold by the RARalpha-selective agonist Am580, in T-47D breast cancer cells. RAR pan-agonists and Am580, but not retinoid X receptors (RXR)-agonists, stimulate the expression of PDCD4 in a wide variety of retinoid-inhibited breast cancer cell lines. RAR-agonists did not induce PDCD4 expression in breast cancer cell lines, which were not growth inhibited by retinoi…
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“its loss is diagnostic for human cancer staging and prognostic for survival in colon, lung, liver, breast, glioma and esophageal cancers (6–11).”
From Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65 (2014) · cites this paper as [6]
In the citing paper
“PDCD4 is a pro-apoptotic tumor suppressor gene and has been verified as a miR-21 target in human colorectal and breast cancer cell lines (Afonja et al., 2004; Asangani et al., 2007; Bitomsky et al., 2008; Frankel et al., 2007; Lu et al., 2008; Zhang et al., 2006).”
From Modulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21 (2010) · cites this paper as Afonja et al., 2004
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Self-citation
Metadata
- Authors
- Afonja, O., Juste, D., Das, S., Matsuhashi, S., & Samuels, H. H.
- Affiliations
- New York University (US)
- Saga University (JP)
- Corresponding author
- Afonja, Olubunmi
- ORCID
- Das, Sharmistha
- Venue
- Oncogene
- Published
- 2004-09-13
- Volume
- 23
- Issue
- 49
- Pages
- 8135-8145
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2071878775
- Cited by
- 154
- References
- 47
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 8 · 2021: 1 · 2020: 5 · 2019: 4 · 2018: 8 · 2017: 7 · 2016: 5 · 2015: 13 · 2014: 13 · 2013: 10 · 2012: 9
- FWCI
- 2.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Robert Wood Johnson Foundation
- National Cancer Institute (K12 CA 01713, K12CA001713)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK16636)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- PDCD4, retinoic acid receptor agonists, breast cancer, apoptosis, tumor suppressor gene expression, antiestrogens, trastuzumab, AM580, retinoids, gene expression profiling, T47D cells, MDA-MB-231 cells, chemoprevention, retinoid X receptor
- MeSH terms
- Breast Neoplasms, Cell Cycle, Estrogen Antagonists, Humans, Transcription Factors, Gene Expression Regulation, Neoplastic, RNA-Binding Proteins, Apoptosis, Receptors, Retinoic Acid, Receptor, ErbB-2, Erb-b2 Receptor Tyrosine Kinases, Cell Line, Tumor, Retinoid X Receptors, Apoptosis Regulatory Proteins
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