The Tumor Suppressor Adenomatous Polyposis Coli and Caudal Related Homeodomain Protein Regulate Expression of Retinol Dehydrogenase L

Jette, Cicely; Peterson, Peter; Sandoval, Imelda T.; Manos, Elizabeth J.; Hadley, E; Ireland, Chris M.; Jones, David A.

doi:10.1074/jbc.m314021200

Cited by 61 publications

(79 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Zebrafish microarrays were obtained from Agilent, and data analysis was performed by using GeneSpring software. The generation of cRNA probes and hybridization to slides were performed according to the manufacturer's protocol (Agilent, Palo Alto, CA) and as described previously (12).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development

Nadauld

Chidester

Shelton

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Congenital hypertrophy͞hyperplasia of the retinal pigmented epithelium is an ocular lesion found in patients harboring mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. We report that Apc-deficient zebrafish display developmental abnormalities of both the lens and retina. Injection of dominantnegative Lef reduced Wnt signaling in the lens but did not rescue retinal differentiation defects. In contrast, treatment of apc mutants with all-trans retinoic acid rescued retinal differentiation defects but had no apparent effect on the lens. We identified Rdh5 as a retina-specific retinol dehydrogenase controlled by APC. Morpholino knockdown of Rdh5 phenocopied the apc mutant retinal differentiation defects and was rescued by treatment with exogenous all-trans retinoic acid. Microarray analyses of apc mutants and Rdh5 morphants revealed a profound overlap in the transcriptional profile of these embryos. These findings support a model wherein Apc serves a dual role in regulating Wnt and retinoic acid signaling within the eye and suggest retinoic acid deficiency as an explanation for APC mutation-associated retinal defects such as congenital hypertrophy͞hyperplasia of the retinal pigmented epithelium.colon cancer ͉ retina ͉ APC

show abstract

Section: Methodsmentioning

confidence: 99%

“…An additional APC function includes its recently described role in regulating the production of retinoic acid (RA) in the intestine (12,13). It is well established that RA is required during eye development (14).…”

mentioning

confidence: 99%

Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development

Nadauld

Chidester

Shelton

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Interestingly, APC control of retinoic acid production seems independent of the canonical model for APC function (19). In the canonical model, APC negatively regulates WNT signaling by helping to target the transcriptional coactivator h-catenin for ubiquitin-mediated proteolysis.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, Jette et al (19) showed that a human retinol dehydrogenase (RDH), DHRS9, is lost in colon tumors compared with normal colon tissue. Moreover, this enzyme was induced upon reintroduction of wild-type APC into colon cancer cell lines, thereby linking APC function with retinoic acid biosynthesis for the first time.…”

Section: Introductionmentioning

confidence: 99%

Up-regulation of CYP26A1 in Adenomatous Polyposis Coli–Deficient Vertebrates via a WNT-Dependent Mechanism: Implications for Intestinal Cell Differentiation and Colon Tumor Development

et al. 2006

Self Cite

View full text Add to dashboard Cite

Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene seem to underlie the initiation of many colorectal carcinomas. Loss of APC function results in accumulation of B-catenin and activation of B-catenin/TCFdependent transcription. Recent studies have implicated APC in controlling retinoic acid biosynthesis during normal intestinal development through a WNT-independent mechanism. Paradoxically, however, previous studies found that dietary supplementation of Apc MIN mice with retinoic acid failed to abrogate adenoma formation. While investigating the above finding, we found that expression of CYP26A1, a major retinoic acid catabolic enzyme, was up-regulated in Apc MIN mouse adenomas, human FAP adenomas, human sporadic colon carcinomas, and in the intestine of apc mcr mutant zebrafish embryos. Mechanistically, cyp26a1 induction following apc mutation is dependent on WNT signaling as antisense morpholino knockdown of tcf4 or injection of a dnLEF construct into apc mcr mutant zebrafish suppressed expression of cyp26a1 along with known WNT target genes. In addition, injection of stabilized b-catenin or dnGSK3b into wild-type embryos induced cyp26a1 expression. Genetic knockdown or pharmacologic inhibition of cyp26a1 in apc mcr mutant zebrafish embryos rescued gut differentiation defects such as expression of intestinal fatty acid-binding protein and pancreatic trypsin. These findings support a novel role for APC in balancing retinoic acid biosynthesis and catabolism through WNT-independent and WNT-dependent mechanisms. (Cancer Res 2006; 66(15): 7571-7)

show abstract

“…Both the reactions are catalyzed by multiple RDH isozymes, including RDH2, RDH10, and DHRS9. Knockout or inadequate expression of individual RDH produces a specific phenotype associated with impaired retinoid function, including enhanced adiposity (mRdh1), defects in head and body development (RDH10), or increased tumorigenesis (DHRS9) [11][12][13] . Three retinaldehyde dehydrogenases (RALDH(s)) have also been associated with generation of atRA, by modifying adiposity (RALDH1) 14 or supporting embryonic development (Raldh -2 and -3) 15,16 .…”

Section: Introductionmentioning

confidence: 99%

Retinol oxidation to retinoic acid in human thyroid glandular cells

Taibi

Gueli

Nicotra

et al. 2014

Journal of Enzyme Inhibition and Medicinal Chemistry

View full text Add to dashboard Cite

Retinoic acid is regarded as the retinol metabolite that controls proliferation and differentiation of epithelial cells. In the present study, we investigated the potential role of xanthine dehydrogenase (XDH) in retinoic acid biosynthesis in human thyroid glandular cells (HTGC). In particular, we observed that cellular retinoids binding proteins (CRBPs) are also implicated in the biosynthetic pathway leading to retinoic acid formation in primary cultures of HTGC, as we have already reported for human mammary epithelial cells (HMEC). After partial protein purification, the enzyme responsible for retinoic acid biosynthesis was identified and quantified as XDH by immunoassay, by its ability to oxidize xanthine to uric acid and its sensitivity to the inhibitory effect of oxypurinol. The evidence of XDH-driven formation of retinoic acid in HTGC cultures further corroborates the potential role of XDH in retinoic acid biosynthesis in the epithelia.

show abstract

The Tumor Suppressor Adenomatous Polyposis Coli and Caudal Related Homeodomain Protein Regulate Expression of Retinol Dehydrogenase L

Cited by 61 publications

References 62 publications

Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development

Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development

Up-regulation of CYP26A1 in Adenomatous Polyposis Coli–Deficient Vertebrates via a WNT-Dependent Mechanism: Implications for Intestinal Cell Differentiation and Colon Tumor Development

Retinol oxidation to retinoic acid in human thyroid glandular cells

Contact Info

Product

Resources

About