Decreased expression of CXXC4 promotes a malignant phenotype in renal cell carcinoma by activating Wnt signaling View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-10-20

AUTHORS

T Kojima, T Shimazui, S Hinotsu, A Joraku, T Oikawa, K Kawai, R Horie, H Suzuki, R Nagashima, K Yoshikawa, T Michiue, M Asashima, H Akaza, K Uchida

ABSTRACT

The Wnt signaling pathway is involved in normal embryonic development and controls the homeostatic self-renewal of stem cells in adult tissues. Constitutive activation of Wnt signaling contributes to cancer development and progression. We identified a CXXC4 homozygous deletion at 4q24 in an aggressive renal cell carcinoma (RCC) using single-nucleotide polymorphism (SNP) arrays. CXXC4 encodes Idax, which negatively regulates Wnt signaling by binding to the PDZ domain of Dishevelled. CXXC4 mRNA levels in tumor samples were significantly lower in patients with metastases compared with those without (P=0.0016). Patients whose tumors had lower CXXC4 expression than normal kidney showed a poorer cause-specific survival outcome than those with higher expression (P=0.0095). Decreased expression of CXXC4 also correlated with cytoplasmic staining of β-catenin. Knockdown of CXXC4 induced the nuclear translocation of β-catenin and altered expression of a set of genes involved in cell proliferation, invasion and survival. Furthermore, reduced expression of CXXC4 by small interfering RNAs promoted cell proliferation and inhibited apoptosis after 5-FU and doxorubicin treatment in RCC cells. These data suggest that CXXC4 plays a critical role in tumor progression of RCC through Wnt signaling. Wnt signaling could thus be a potential molecular target in RCC indicating decreased CXXC4 expression. More... »

PAGES

297-305

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2008.391

DOI

http://dx.doi.org/10.1038/onc.2008.391

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022531101

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18931698


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