ArticleThe Journal of biological chemistry2014
Transcriptional repression of tumor suppressor CDC73, encoding an RNA polymerase II interactor, by Wilms tumor 1 protein (WT1) promotes cell proliferation: implication for cancer therapeutics.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Current Knowledge on Atypical Parathyroid Tumors and Emerging Strategies for Risk Stratification.Endocrinology and metabolism (Seoul, Korea) · 2026Review
- WT1 gene: a potential therapeutic target for multiple cancer treatment strategies.Clinical and experimental medicine · 2025Review
- Transcriptome sequencing reveals distinct atypical parathyroid tumor subtypes.Endocrine-related cancer · 2025Article
- Phenotypic Profiling and Molecular Mechanisms in Hyperparathyroidism-jaw Tumor Syndrome.The Journal of clinical endocrinology and metabolism · 2023Article
- Genomic and transcriptomic profiling reveal molecular characteristics of parathyroid carcinoma.Experimental & molecular medicine · 2023Article
- Association Between Parafibromin Expression and Presence of Brown Tumors and Jaw Tumors in Patients with Primary Hyperparathyroidism: Series of Cases with Review of the Literature.The American journal of case reports · 2022Review
- UBR5 targets tumor suppressor CDC73 proteolytically to promote aggressive breast cancer.Cell death & disease · 2022Article
- The roles of the tumor suppressor parafibromin in cancer.Frontiers in cell and developmental biology · 2022Review
- RNA m6A methylation regulators in ovarian cancer.Cancer cell international · 2021Review
- Network pharmacology based research into the effect and mechanism of Yinchenhao Decoction against Cholangiocarcinoma.Chinese medicine · 2021Article
- Circular RNA_0000629 Suppresses Bladder Cancer Progression Mediating MicroRNA-1290/CDC73.Cancer management and research · 2021Article
- WT1 facilitates the self-renewal of leukemia-initiating cells through the upregulation of BCL2L2: WT1-BCL2L2 axis as a new acute myeloid leukemia therapy target.Journal of translational medicine · 2020Article
- Circ_0000140 restrains the proliferation, metastasis and glycolysis metabolism of oral squamous cell carcinoma through upregulating CDC73 via sponging miR-182-5p.Cancer cell international · 2020Article
- A Unique Family of Neuronal Signaling Proteins Implicated in Oncogenesis and Tumor Suppression.Frontiers in oncology · 2019Review
- Co-sequencing and novel delayed anti-correlation identify function for pancreatic enriched microRNA biomarkers in a rat model of acute pancreatic injury.BMC genomics · 2018Article
- Large intragenic deletion of CDC73 (exons 4-10) in a three-generation hyperparathyroidism-jaw tumor (HPT-JT) syndrome family.BMC medical genetics · 2017Article
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- The roles of parafibromin expression in ovarian epithelial carcinomas: a marker for differentiation and prognosis and a target for gene therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Overexpression of PD2 leads to increased tumorigenicity and metastasis in pancreatic ductal adenocarcinoma.Oncotarget · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wilms tumor 1 gene (WT1) can either repress or induce the expression of genes. Inconsistent with its tumor suppressor role, elevated WT1 levels have been observed in leukemia and solid tumors. WT1 has also been suggested to act as an oncogene by inducing the expression of MYC and BCL-2. However, these are only the correlational studies, and no functional study has been performed to date. Consistent with its tumor suppressor role, CDC73 binds to RNA polymerase II as part of a PAF1 transcriptional regulatory complex and causes transcriptional repression of oncogenes MYC and CCND1. It also represses β-catenin-mediated transcription. Based on the reduced level of CDC73 in oral squamous cell carcinoma (OSCC) samples in the absence of loss-of-heterozygosity, promoter methylation, and mutations, we speculated that an inhibitory transcription factor is regulating its expression. The bioinformatics analysis predicted WT1 as an inhibitory transcription factor to regulate the CDC73 level. Our results showed that overexpression of WT1 decreased CDC73 levels and promoted proliferation of OSCC cells. ChIP and EMSA results demonstrated binding of WT1 to the CDC73 promoter. The 5-azacytidine treatment of OSCC cells led to an up-regulation of WT1 with a concomitant down-regulation of CDC73, further suggesting regulation of CDC73 by WT1. Exogenous CDC73 attenuated the protumorigenic activity of WT1 by apoptosis induction. An inverse correlation between expression levels of CDC73 and WT1 was observed in OSCC samples. These observations indicated that WT1 functions as an oncogene by repressing the expression of CDC73 in OSCC. We suggest that targeting WT1 could be a therapeutic strategy for cancer, including OSCC.
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