ArticleClinical epigenetics2019
Epigenetic therapy of novel tumour suppressor ZAR1 and its cancer biomarker function.
Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026Review
- A Bioinformatics and Wet-Lab-Based Pipeline IdentifiesInternational journal of molecular sciences · 2026Article
- The Regulation of ZAR1 on Apoptosis and Mitophagy in Ovarian Granular Cells and Primary Ovarian Insufficiency (POI) Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Epigenetic silencing and CRISPR-mediated reactivation of tight junction protein claudin10b (CLDN10B) in renal cancer.Clinical epigenetics · 2025Article
- SIAH3 is frequently epigenetically silenced in cancer and regulates mitochondrial metabolism.International journal of cancer · 2025Article
- The tumor suppressor FAT1 controls YAP/TAZ protein degradation and tumor cell proliferation through E3 ligase MIB2.PloS one · 2025Article
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- Assay for Transposase-Accessible Chromatin Using Sequencing of Freshly Isolated Muscle Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Low expression of PRDM5 predicts poor prognosis of esophageal squamous cell carcinoma.BMC cancer · 2022Article
- Epigenetic Editing in Prostate Cancer: Challenges and Opportunities.Epigenetics · 2022Review
- First-in-human study of inhaled Azacitidine in patients with advanced non-small cell lung cancer.Lung cancer (Amsterdam, Netherlands) · 2021Article
- Epigenetic Inactivation of the Tumor SuppressorCancers · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer still is one of the leading causes of death and its death toll is predicted to rise further. We identified earlier the potential tumour suppressor zygote arrest 1 (ZAR1) to play a role in lung carcinogenesis through its epigenetic inactivation.
resultsWe are the first to report that ZAR1 is epigenetically inactivated not only in lung cancer but also across cancer types, and ZAR1 methylation occurs across its complete CpG island. ZAR1 hypermethylation significantly correlates with its expression reduction in cancers. We are also the first to report that ZAR1 methylation and expression reduction are of clinical importance as a prognostic marker for lung cancer and kidney cancer. We further established that the carboxy (C)-terminally present zinc-finger of ZAR1 is relevant for its tumour suppression function and its protein partner binding associated with the mRNA/ribosomal network. Global gene expression profiling supported ZAR1's role in cell cycle arrest and p53 signalling pathway, and we could show that ZAR1 growth suppression was in part p53 dependent. Using the CRISPR-dCas9 tools, we were able to prove that epigenetic editing and reactivation of ZAR1 is possible in cancer cell lines.
conclusionZAR1 is a novel cancer biomarker for lung and kidney, which is epigenetically silenced in various cancers by DNA hypermethylation. ZAR1 exerts its tumour suppressive function in part through p53 and through its zinc-finger domain. Epigenetic therapy can reactivate the ZAR1 tumour suppressor in cancer.
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