ArticleCancer research2016
Transcription Factor ZBP-89 Drives a Feedforward Loop of β-Catenin Expression in Colorectal Cancer.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Integrating machine learning with SHAP to uncover multi-tissue molecular signatures in Osteoarthritis progression.PloS one · 2026Article
- Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1.Oncology reports · 2024Article
- ZNF148 inhibits HBV replication by downregulating RXRα transcription.Virology journal · 2024Article
- Peripheral Blood Mononuclear Cell Biomarkers for Major Depressive Disorder: A Transcriptomic Approach.Depression and anxiety · 2024Article
- Upregulation of the ZNF148/PTX3 axis promotes malignant transformation of dendritic cells in glioma stem-like cells microenvironment.CNS neuroscience & therapeutics · 2023Article
- The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023Review
- A MYC-ZNF148-ID1/3 regulatory axis modulating cancer stem cell traits in aggressive breast cancer.Oncogenesis · 2022Article
- β Cell-specific deletion of Zfp148 improves nutrient-stimulated β cell Ca2+ responses.JCI insight · 2022Article
- RNA mMolecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Single allele loss-of-function mutations select and sculpt conditional cooperative networks in breast cancer.Nature communications · 2021Article
- Identification of ZBTB18 as a novel colorectal tumor suppressor gene through genome-wide promoter hypermethylation analysis.Clinical epigenetics · 2021Article
- Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway.Scientific reports · 2020Article
- ZBP-89 negatively regulates self-renewal of liver cancer stem cells via suppression of Notch1 signaling pathway.Cancer letters · 2020Article
- Construction of an Immunogenomic Risk Score for Prognostication in Colon Cancer.Frontiers in genetics · 2020Article
- Peritumoral overexpression of ZBP-89 is associated with unfavorable disease-free survival rates in patients with hepatocellular carcinoma following hepatectomy.Oncology letters · 2018Article
- Modulating the expression of Chtop, a versatile regulator of gene-specific transcription and mRNA export.RNA biology · 2018Review
- Article
- STRAP Promotes Stemness of Human Colorectal Cancer via Epigenetic Regulation of the NOTCH Pathway.Cancer research · 2017Article
- Zinc-finger proteins in health and disease.Cell death discovery · 2017Review
- ZNF148 modulates TOP2A expression and cell proliferation via ceRNA regulatory mechanism in colorectal cancer.Medicine · 2017Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
In colorectal cancer, APC-mediated induction of unregulated cell growth involves posttranslational mechanisms that prevent proteasomal degradation of proto-oncogene β-catenin (CTNNB1) and its eventual translocation to the nucleus. However, about 10% of colorectal tumors also exhibit increased CTNNB1 mRNA. Here, we show in colorectal cancer that increased expression of ZNF148, the gene coding for transcription factor ZBP-89, correlated with reduced patient survival. Tissue arrays showed that ZBP-89 protein was overexpressed in the early stages of colorectal cancer. Conditional deletion of Zfp148 in a mouse model of Apc-mediated intestinal polyps demonstrated that ZBP-89 was required for polyp formation due to induction of Ctnnb1 gene expression. Chromatin immunoprecipitation (ChIP) and EMSA identified a ZBP-89-binding site in the proximal promoter of CTNNB1 Reciprocally, siRNA-mediated reduction of CTNNB1 expression also decreased ZBP-89 protein. ChIP identified TCF DNA binding sites in the ZNF148 promoter through which Wnt signaling regulates ZNF148 gene expression. Suppression of either ZNF148 or CTNNB1 reduced colony formation in WNT-dependent, but not WNT-independent cell lines. Therefore, the increase in intracellular β-catenin protein initiated by APC mutations is sustained by ZBP-89-mediated feedforward induction of CTNNB1 mRNA. Cancer Res; 76(23); 6877-87. ©2016 AACR.
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