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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PDCD4 loss is diagnostic for human cancer staging and prognostic for survival in colon, lung, liver, breast, glioma and esophageal cancers.
“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]
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.
“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
- 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 › Genetics › 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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