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CDX2 is a transcription factor involved in human intestine development and function. It is also utilized as a marker of differentiation in early lesions and cancers of the intestine, stomach, and liver [154],[155]. CDX2 controls intestinal stem cell development and function, and it is also involved in intestine tumorigenesis [154],[155]. When CDX2 is overexpressed or mutated, cells become resistant to growth inhibition and apoptosis. The N-terminal domain of CDX2 is necessary for ligand-dependent transcriptional activation [154],[155]. The transcriptional repression domain is located in the C-terminal region of CDX2. Transcriptional repression requires the binding of Groucho proteins and epigenetic modifications such as H3K9me2 [154],[155]. CDX2 C-terminal repression domain (CTRD) mutants enhance the tumorigenic potential of colon cancer cells through increased nuclear localization of β-catenin/TCF4 [156] [157]. Wang et al. hypothesized that these effects are mediated by the upregulation of the Wnt target genes c-myc and cyclin D1. Wang et al. found that the upregulation of c-myc is a direct target of Wnt signaling in colon cancer cell lines. Furthermore, when a CDX2 mutant with an intact C-terminal region was transiently over-expressed, the Wnt target gene c-myc was upregulated. This indicates that the C-terminal domain of CDX2 functions to repress c-myc expression in colon cancer cells [158]. However, CDX2 does not repress c-myc expression in normal cells. Finally, they tested CDX2 in a rhesus macaque model of human colon cancer. They used an HDAd5/3 vector, which contains only Ad5 and Ad3 fiber proteins and was previously shown to be safe and efficient in rodents, non-human primates, and humans [159],[160]. Using CDX2-expressing HDAd5/3, they found that it can undergo both viral and cellular uptake. Importantly, by contrast to wild-type CDX2, CDX2-expressing HDAd5/3 did not localize to the nucleus and did not induce apoptosis.
Uterine cervix cancers contain over 60 different subtypes, and most current therapies target the EGF receptor or downstream pathways. In an analysis of tumor biopsies from 95 patients with cervical cancer, the expression of Wnt1 and Frizzled4 was detected in 63% of uterine cervix cancers [136]. The Wnt/Frizzled pathway was also activated in gynecologic cancers, and the Wnt inhibitors APC and beta-catenin are expressed in cervical cancer, but not in normal cervical epithelium. In a small phase I study of women with advanced cervical cancer, a combination of anti-Frizzled4 antibody and beta-catenin antagonist was tested, and both agents were well-tolerated [137].
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