ArticleOncotarget2017
Silencing PRDM14 expression by an innovative RNAi therapy inhibits stemness, tumorigenicity, and metastasis of breast cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Interaction Between PRDM14 and CBFA2T2 Supports Pluripotency and Proliferation in Germ Cell Tumors.Cancers · 2026Article
- The role of HOXA1 in cancer and targeted therapy.Medical oncology (Northwood, London, England) · 2025Review
- Antitumoral RNA-targeted oligonucleotide therapeutics: The third pillar after small molecule inhibitors and antibodies.Cancer science · 2022Review
- The duality of PRDM proteins: epigenetic and structural perspectives.The FEBS journal · 2022Review
- Therapeutic siRNA targeting the cancer cell stemness regulator PRDI-BF1 and RIZ domain zinc finger protein 14.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022Article
- Histone 3 Lysine 27 Trimethylation Signature in Breast Cancer.International journal of molecular sciences · 2021Review
- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
- Immune-related protein signature in serum stratify relapsed mantle cell lymphoma patients based on risk.BMC cancer · 2020Article
- Epithelial-Mesenchymal Transition Programs and Cancer Stem Cell Phenotypes: Mediators of Breast Cancer Therapy Resistance.Molecular cancer research : MCR · 2020Review
- PRDM14 promotes malignant phenotype and correlates with poor prognosis in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14.Trends in genetics : TIG · 2019Review
- The Pluripotency Regulator PRDM14 Requires Hematopoietic Regulator CBFA2T3 to Initiate Leukemia in Mice.Molecular cancer research : MCR · 2019Article
- The Evolving Landscape of Cancer Stem Cells and Ways to Overcome Cancer Heterogeneity.Cancers · 2019Review
- Integrated Analysis of Genetic Abnormalities of the Histone Lysine Methyltransferases in Prostate Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Targeted DamID reveals differential binding of mammalian pluripotency factors.Development (Cambridge, England) · 2018Article
- PRDM14 is overexpressed in chronic pancreatitis prior to pancreatic cancer.FEBS open bio · 2018Article
- PRDM14 directly interacts with heat shock proteins HSP90α and glucose-regulated protein 78.Cancer science · 2018Article
- Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials.Signal transduction and targeted therapyReview
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PR domain zinc finger protein 14 (PRDM14) maintains stemness in embryonic stem cells via epigenetic mechanisms. Although PRDM14 is elevated in several cancers, it is unclear if and how PRDM14 confers stem cell-like properties and epigenetic changes to cancer cells. Here, we examined the phenotypic characteristics and epigenetic and gene expression profiles of cancer cells that differentially express PRDM14, and assessed the potential of PRDM14-targeted cancer therapy. PRDM14 expression was markedly increased in many different cancer types and correlated with poor survival of breast cancer patients. PRDM14 conferred stem cell-like phenotypes to cancer cells and regulated the expression of genes involved in cancer stemness, metastasis, and chemoresistance. PRDM14 also reduced the methylation of proto-oncogene and stemness gene promoters and PRDM14-binding regions were primarily occupied by histone H3 Lys-4 trimethylation (H3K4me3), both of which are positively correlated with gene expression. Moreover, strong PRDM14 binding sites coincided with promoters containing both H3K4me3 and H3K27me3 histone marks. Using calcium phosphate hybrid micelles as an RNAi delivery system, silencing of PRDM14 expression by chimera RNAi reduced tumor size and metastasis in vivo without causing adverse effects. Conditional loss of PRDM14 function also improved survival of MMTV-Wnt-1 transgenic mice, a spontaneous model of murine breast cancer. Our findings suggest that PRDM14 inhibition may be an effective and novel therapy for cancer stem cells.
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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.