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Gene Review

Wt1  -  Wilms tumor 1

Rattus norvegicus

Synonyms: Wilms tumor protein homolog, Wt-1
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Disease relevance of Wt1


High impact information on Wt1

  • A dominant mutation in the Wilms tumor gene WT1 cooperates with the viral oncogene E1A in transformation of primary kidney cells [3].
  • Wilms' tumor (WT), the embryonic kidney malignancy, is suggested to evolve from a progenitor cell population of uninduced metanephric blastema, which typically gives rise to nephrons [2].
  • Thus, multiple imprinted and stemness genes that function to expand the renal progenitor cell population may lead to evolution and maintenance of WT [2].
  • However, apart from blastema, WT specimens frequently contain cells that have differentiated into renal tubular or stromal phenotypes, complicating their analysis [2].
  • The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors [4].

Chemical compound and disease context of Wt1

  • We show here that Wt1 mRNA and protein is up-regulated in the heart and kidneys of rats exposed to normobaric hypoxia (8% O2) [1].
  • PPARgamma expression in CONT at 12 weeks was increased in podocytes and in mesangial WT-1 cells in segmentally sclerotic glomeruli, with less Wilms' tumor 1 (WT-1) staining [5].

Biological context of Wt1

  • Assignment of the Wilms' tumor (Wt1) gene to rat chromosome bands 3q34-->q35 by in situ hybridization [6].
  • Our results indicate that impairment of DNA binding of the WT1 tumor-suppressor gene product can result in a dominant negative mutation [3].
  • WT1, a gene deleted in some Wilms' tumors, encodes a transcription factor with zinc fingers and shares homology with proteins in the early growth response gene family [7].
  • Cotransfection of a WT1 expression vector with a promoter reporter plasmid of inhibin-alpha resulted in the repression of promoter activities in CHO cells in a dose-dependent manner [7].
  • In addition, the actions of p53 may be amplified through a cooperative interaction with another tumor suppressor protein, the product of the Wilms' tumor suppressor gene (WT-1) [8].

Anatomical context of Wt1

  • We recently described de novo expression of Wt1 in myocardial blood vessels of ischemic rat hearts [1].
  • In P6 rats, mesangial WT-1 staining was lessened, but podocyte staining was strongly accentuated [5].
  • These results suggest that WT1 is expressed in high levels in granulosa cells of primordial, primary, and secondary follicles but decreases with follicle development [7].
  • We have previously shown that expression of the WT1(-/-) isoform, lacking both inserts, increases the tumor growth rate of the adenovirus-transformed baby rat kidney (AdBRK) cell line 7C3H2, whereas expression of the WT1(-/+) isoform, lacking the 17aa insert, strongly suppresses the tumorigenic phenotype [4].
  • Abundant WT1 transcripts were found in the ovary, testis, uterus, and kidney, with lower levels in the heart and pancreas [7].

Associations of Wt1 with chemical compounds


Other interactions of Wt1

  • Ectopic Wt1 immunoreactivity was detected in renal tubules of hypoxic rats, which also expressed the antiapoptotic protein Bcl-2 and contained significantly fewer TUNEL-positive cells than in normoxic kidneys [1].

Analytical, diagnostic and therapeutic context of Wt1

  • We aimed to define tumor-progenitor genes that function in normal kidney development using WT xenografts (WISH-WT), in which the blastema accumulates with serial passages at the expense of differentiated cells [2].
  • We investigated the expression of WT1 transcripts in rat ovary during follicle development by Northern blotting, RNase protection assay, and in situ hybridization [7].
  • Subcutaneous injection of immature rats with 10 IU equine CG (eCG) reduced the levels of p53 and WT-1 mRNA to 71 +/- 9% (P < 0.05) and 46 +/- 3% (P < 0.05), respectively, of saline-treated control levels after 2 days [8].
  • Unilateral nephrectomy induces the expression of the Wilms tumor gene in the contralateral kidney of the adult rat [10].
  • Receptors on tumor cells bind factors which, when eluted followed by in vivo bioassay, stimulate the growth of Wilms tumor [11].


  1. Oxygen-regulated expression of the Wilms' tumor suppressor Wt1 involves hypoxia-inducible factor-1 (HIF-1). Wagner, K.D., Wagner, N., Wellmann, S., Schley, G., Bondke, A., Theres, H., Scholz, H. FASEB J. (2003) [Pubmed]
  2. Multiple imprinted and stemness genes provide a link between normal and tumor progenitor cells of the developing human kidney. Dekel, B., Metsuyanim, S., Schmidt-Ott, K.M., Fridman, E., Jacob-Hirsch, J., Simon, A., Pinthus, J., Mor, Y., Barasch, J., Amariglio, N., Reisner, Y., Kaminski, N., Rechavi, G. Cancer Res. (2006) [Pubmed]
  3. A dominant mutation in the Wilms tumor gene WT1 cooperates with the viral oncogene E1A in transformation of primary kidney cells. Haber, D.A., Timmers, H.T., Pelletier, J., Sharp, P.A., Housman, D.E. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  4. EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity. Scharnhorst, V., Menke, A.L., Attema, J., Haneveld, J.K., Riteco, N., van Steenbrugge, G.J., van der Eb, A.J., Jochemsen, A.G. Oncogene (2000) [Pubmed]
  5. Peroxisome proliferator-activated receptor-gamma agonist is protective in podocyte injury-associated sclerosis. Yang, H.C., Ma, L.J., Ma, J., Fogo, A.B. Kidney Int. (2006) [Pubmed]
  6. Assignment of the Wilms' tumor (Wt1) gene to rat chromosome bands 3q34-->q35 by in situ hybridization. Kindler-Röhrborn, A., Zabel, S., Koelsch, B.U. Cytogenet. Cell Genet. (2000) [Pubmed]
  7. Wilms' tumor protein WT1 as an ovarian transcription factor: decreases in expression during follicle development and repression of inhibin-alpha gene promoter. Hsu, S.Y., Kubo, M., Chun, S.Y., Haluska, F.G., Housman, D.E., Hsueh, A.J. Mol. Endocrinol. (1995) [Pubmed]
  8. Expression of the p53 and Wilms' tumor suppressor genes in the rat ovary: gonadotropin repression in vivo and immunohistochemical localization of nuclear p53 protein to apoptotic granulosa cells of atretic follicles. Tilly, K.I., Banerjee, S., Banerjee, P.P., Tilly, J.L. Endocrinology (1995) [Pubmed]
  9. Dietary alpha-tocopherol affects differential gene expression in rat testes. Rota, C., Barella, L., Minihane, A.M., Stöcklin, E., Rimbach, G. IUBMB Life (2004) [Pubmed]
  10. Unilateral nephrectomy induces the expression of the Wilms tumor gene in the contralateral kidney of the adult rat. Siegel, J.F., Delakas, D., Rai, S., Kushner, L. J. Urol. (1996) [Pubmed]
  11. Specificity of renotropin receptors in murine Wilms tumor model. Tritsch, G.L., Williams, P.D., Sufrin, G., Murphy, G.P. Urology (1985) [Pubmed]
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