ArticleOncotarget2016
Targeting Zfp148 activates p53 and reduces tumor initiation in the gut.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Hsa_circRNA_0101125 Promotes Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma via miR-143-3p/ZNF148 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Targeting the ZNF-148/miR-335/SOD2 signaling cascade triggers oxidative stress-mediated pyroptosis and suppresses breast cancer progression.Cancer medicine · 2023Article
- Article
- SGOL2 is a novel prognostic marker and fosters disease progression via a MAD2-mediated pathway in hepatocellular carcinoma.Biomarker research · 2022Article
- β Cell-specific deletion of Zfp148 improves nutrient-stimulated β cell Ca2+ responses.JCI insight · 2022Article
- Antioxidants Promote Intestinal Tumor Progression in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway.Scientific reports · 2020Article
- Peritumoral overexpression of ZBP-89 is associated with unfavorable disease-free survival rates in patients with hepatocellular carcinoma following hepatectomy.Oncology letters · 2018Article
- Article
- Transcription Factor ZBP-89 Drives a Feedforward Loop of β-Catenin Expression in Colorectal Cancer.Cancer research · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Zinc finger protein 148 (Zfp148, ZBP-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53, but the significance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in some tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity. Here we hypothesize that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas. Loss of one copy of Zfp148 markedly reduced tumor numbers and tumor-associated intestinal bleedings, and improved survival. Furthermore, after activation of β-catenin-the initiating event in colorectal cancer-Zfp148 deficiency activated p53 and induced apoptosis in intestinal explants of APCMin/+ mice. The anti-tumor effect of targeting Zfp148 depended on p53, as Zfp148 deficiency did not affect tumor numbers in APCMin/+ mice lacking one or both copies of Trp53. The results suggest that Zfp148 controls the fate of newly transformed intestinal tumor cells by repressing p53 and that targeting Zfp148 might be useful in the treatment of colorectal cancer.
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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.