ArticleJournal of cellular biochemistry2009
PDEF is a negative regulator of colon cancer cell growth and migration.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Assessing the Tumor Suppressive Impact and Regulatory Mechanisms of SPDEF Expression in Breast Cancer.Cancers · 2025Article
- SPDEF enhances cancer stem cell-like properties and tumorigenesis through directly promoting GALNT7 transcription in luminal breast cancer.Cell death & disease · 2023Article
- Neuroplastinβ-mediated upregulation of solute carrier family 22 member 18 antisense (SLC22A18AS) plays a crucial role in the epithelial-mesenchymal transition, leading to lung cancer cells' enhanced motility.Biochemistry and biophysics reports · 2020Article
- Upregulation of SPDEF is associated with poor prognosis in prostate cancer.Oncology letters · 2019Article
- AR-PDEF pathway promotes tumour proliferation and upregulates MYC-mediated gene transcription by promoting MAD1 degradation in ER-negative breast cancer.Molecular cancer · 2018Article
- ELF3, ELF5, EHF and SPDEF Transcription Factors in Tissue Homeostasis and Cancer.Molecules (Basel, Switzerland) · 2018Review
- Prostate-derived ETS factor improves prognosis and represses proliferation and invasion in hepatocellular carcinoma.Oncotarget · 2017Article
- SPDEF Induces Quiescence of Colorectal Cancer Cells by Changing the Transcriptional Targets of β-catenin.Gastroenterology · 2017Article
- The androgen-induced protein AIbZIP facilitates proliferation of prostate cancer cells through downregulation of p21 expression.Scientific reports · 2016Article
- Signatures of prostate-derived Ets factor (PDEF) in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- GADD45α and γ interaction with CDK11p58 regulates SPDEF protein stability and SPDEF-mediated effects on cancer cell migration.Oncotarget · 2016Article
- Article
- Silencing of the EPHB3 tumor-suppressor gene in human colorectal cancer through decommissioning of a transcriptional enhancer.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Identification of upstream regulators for prognostic expression signature genes in colorectal cancer.BMC systems biology · 2013Article
- PDEF promotes luminal differentiation and acts as a survival factor for ER-positive breast cancer cells.Cancer cell · 2013Article
- SPDEF functions as a colorectal tumor suppressor by inhibiting β-catenin activity.Gastroenterology · 2013Article
- Understanding the role of ETS-mediated gene regulation in complex biological processes.Advances in cancer research · 2013Review
- The transcription factor SPDEF suppresses prostate tumor metastasis.The Journal of biological chemistry · 2012Article
- Mechanisms and functional consequences of PDEF protein expression loss during prostate cancer progression.The Prostate · 2011Article
- Prostate-derived Ets transcription factor (PDEF) is a potential prognostic marker in patients with prostate cancer.The Prostate · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
ETS is a family of transcriptional regulators with functions in most biological processes. Dysregulated ETS factor function leads to altered expression of multiple genes that play critical roles in many of the processes required for cancer progression. While the Ets family gene, prostate-derived ETS factor (PDEF), is expressed in epithelial tissues including prostate, breast, and colon, PDEF protein expression has been found to be reduced or lost during prostate and breast cancer progression. The goal of this study was to examine the expression and biologic impact of altered PDEF expression in colon cancer. PDEF mRNA and protein are not detectable in several colon-cancer-derived cell lines. Re-expression of PDEF in colon cancer cells inhibits growth and migration. Growth affects are due to altered cellular proliferation, indicated by increased altered cell population in G(1) and S phases of the cell cycle, as well as increased apoptosis. Relevant to its modulation of growth and migration phenotypes, PDEF expression resulted in altered expression of genes with established roles in cell cycle, motility, and invasion. Furthermore, chromatin immunoprecipitation studies show that p21 and urokinase plasminogen activator (uPA) are direct PDEF transcriptional targets. While non-tumor colon epithelium expresses PDEF mRNA and protein, the majority of tumors showed decreased mRNA and/or protein expression. In human tumor tissue samples, PDEF expression was inversely correlated with the expression levels of uPA. Collectively, the data support the model that PDEF is a negative regulator of tumor progression by modulating the expression of growth and migration promoting genes.
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