ArticleNeoplasia (New York, N.Y.)2008
A pathologic link between Wilms tumor suppressor gene, WT1, and IFI16.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Retinoic acid promotes differentiation of WiT49- but not of CCG99-11 Wilms tumour cells.Cancer reports (Hoboken, N.J.) · 2023Article
- Interferon-induced protein 16 expression in colorectal cancer and its correlation with proliferation and immune signature markers.Oncology letters · 2021Article
- MYCN gene polymorphisms and Wilms tumor susceptibility in Chinese children.Journal of clinical laboratory analysis · 2019Article
- DNA hydroxymethylation profiling reveals that WT1 mutations result in loss of TET2 function in acute myeloid leukemia.Cell reports · 2014Article
- Mechanisms of transcriptional regulation by WT1 (Wilms' tumour 1).The Biochemical journal · 2014Review
- Article
- Dependence of Wilms tumor cells on signaling through insulin-like growth factor 1 in an orthotopic xenograft model targetable by specific receptor inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Functional characterization of Wilms tumor-suppressor WTX and tumor-associated mutants.Oncogene · 2011Article
- Dinosaurs and ancient civilizations: reflections on the treatment of cancer.Neoplasia (New York, N.Y.) · 2010Article
- The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009Article
- An integrated genome screen identifies the Wnt signaling pathway as a major target of WT1.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Dynamic interaction between WT1 and BASP1 in transcriptional regulation during differentiation.Nucleic acids research · 2009Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
- WT1 induction of mitogen-activated protein kinase phosphatase 3 represents a novel mechanism of growth suppression.Molecular cancer research : MCR · 2008Article
Corrections and comments
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Authors and funding
9 authors at 8 institutions in 2 countries.
Funding
Abstract
The Wilms tumor gene (WT1) is mutated or deleted in patients with heredofamilial syndromes associated with the development of Wilms tumors, but is infrequently mutated in sporadic Wilms tumors. By comparing the microarray profiles of syndromic versus sporadic Wilms tumors and WT1-inducible Saos-2 osteosarcoma cells, we identified interferon-inducible protein 16 (IFI16), a transcriptional modulator, as a differentially expressed gene and a candidate WT1 target gene. WT1 induction in Saos-2 osteosarcoma cells led to strong induction of IFI16 expression and its promoter activity was responsive to the WT1 protein. Immunohistochemical analysis showed that IFI16 and WT1 colocalized in WT1-replete Wilms tumors, but not in normal human midgestation fetal kidneys, suggesting that the ability of WT1 to regulate IFI16 in tumors represented an aberrant pathologic relationship. In addition, endogenous IFI16 and WT1 interacted in vivo in two Wilms tumor cell lines. Furthermore, IFI16 augmented the transcriptional activity of WT1 on both synthetic and physiological promoters. Strikingly, short hairpin RNA (shRNA)-mediated knockdown of either IFI16 or WT1 led to decreased growth of Wilms tumor cells. These data suggest that IFI16 and WT1, in certain cellular context including sporadic Wilms tumors, may support cell survival.
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