Wnt Signaling in Renal Cancer

Guillen-Ahlers, Hector

doi:10.2174/138945008784911813

Cited by 41 publications

(26 citation statements)

References 106 publications

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“…The Wnt pathway is activated in a wide variety of tumors such as prostate cancer (40), renal cancer (41), ovarian cancer (42), and EC (19). Wang et al,(43) reported that progesterone inhibits Wnt signaling in the human endometrium through induction of DKK1 and FOXO1.…”

Section: Discussionmentioning

confidence: 99%

Genomic Characterization of Gene Copy-Number Aberrations in Endometrial Carcinoma Cell Lines Derived from Endometrioid-Type Endometrial Adenocarcinoma

Wang

Yang

Cogdell

et al. 2010

Technol Cancer Res Treat

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Endometrial carcinoma is one of the most common cancers in women. A limited number of endometrial carcinoma cell lines are available for studies of signal transduction pathways and experimental therapeutics in vitro. However, these cell lines have not been comprehensively characterized. In this study, we used genome-wide microarray-based comparative genomic hybridization (aCGH) technology to characterize five of the more commonly used endometrial cancer cell lines. We detected DNA copy–number gains in chromosomal regions 2q, 3p, 3q, 5q, 7p, 17q, and19q in all five cell lines. Other common sites of copy–number gains, which were detected in four of five cell lines, included segments of chromosomes 1, 6, 8, 9, 11, 12, and 16. In all five cell lines, we found DNA copy–number losses in regions 3p, 10p, 10q, 11q, 11p, 14q, 15q, 18p, and 21q. Other common sites of genetic aberrations included segments of chromosomes 1, 2, 4, 5, 6, 16, 20, and 22. The genes involved in the copy-number alterations included the oncogenes PIK3CA (3q26.3), K-ras (12p12.1), R-ras (19q13.3-qter), Raf-1 (3p25), EGFR (7p12), Akt1 (14q32.32), and Akt2 (19q13.1-q13.2). A pathway analysis showed that genes in the PI3K and Wnt pathways are commonly affected. Our characterization of genomic alterations in these five commonly used endometrial cancer cell lines provides valuable genomic information for research that focuses on these key oncogenic pathways in endometrial cancer.

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Section: Discussionmentioning

confidence: 99%

Genomic Characterization of Gene Copy-Number Aberrations in Endometrial Carcinoma Cell Lines Derived from Endometrioid-Type Endometrial Adenocarcinoma

Wang

Yang

Cogdell

et al. 2010

Technol Cancer Res Treat

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“…Kurose et al (2004) reported a high incidence of DKK-3 silencing specifically in RCC, suggesting that DKKs also possess tumor suppressor activity. A recent and comprehensive review of Wnt signaling in renal cancer is available (Guillen-Ahlers, 2008). …”

Section: Key Moleculesmentioning

confidence: 99%

VHL loss of function and its impact on oncogenic signaling networks in clear cell renal cell carcinoma

Linehan

Rubin

Bottaro

2009

The International Journal of Biochemistry & Cell Biology

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Loss of von Hippel-Lindau tumor suppressor gene function occurs in familial and most sporadic clear cell renal cell carcinoma, resulting in the aberrant expression of genes that control cell proliferation, metabolism, invasion and angiogenesis. The molecular mechanisms by which loss of function leads to tumorigenesis are not yet fully defined. The von Hippel-Lindau gene product is part of an ubiquitin ligase complex that targets hypoxia inducible factors for polyubiquitination and proteasomal degradation, linking hypoxia response genes to renal cell carcinoma oncogenesis. Loss von Hippel-Lindau gene function also promotes cell invasiveness in response to hepatocyte growth factor, an important regulator of kidney development and renal homeostasis. Increased cell invasiveness is mediated by another ubiquitin ligase target with relevance to the molecular pathogenesis of renal cell carcinoma: β-catenin. This discovery and other recent insights into kidney cancer oncogenesis implicate convergent developmental and homeostatic signaling pathways in tumorigenesis, tumor invasiveness and metastasis.

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“…14, 15, 16, 17, 18 In CRC, adenomatous polyposis coli (APC) is the key tumour suppressor protein and is mutated in ∼80% of sporadic cancers. Moreover, germline heterozygosity of this gene leads to familial adenomatous polyposis (FAP).…”

Section: Introductionmentioning

confidence: 99%

Acute WNT signalling activation perturbs differentiation within the adult stomach and rapidly leads to tumour formation

et al. 2012

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A role for WNT signalling in gastric carcinogenesis has been suggested due to two major observations. First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stomach polyps and second, in gastric cancer, WNT activation confers a poor prognosis. However, the functional significance of deregulated WNT signalling in gastric homoeostasis and cancer is still unclear. In this study we have addressed this by investigating the immediate effects of WNT signalling activation within the stomach epithelium. We have specifically activated the WNT signalling pathway within the mouse adult gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expression of a constitutively active β-catenin protein. WNT pathway deregulation dramatically affects stomach homoeostasis at very short latencies. In the corpus, there is rapid loss of parietal cells with fundic gland polyp (FGP) formation and adenomatous change, which are similar to those observed in familial adenomatous polyposis. In the antrum, adenomas occur from 4 days post-WNT activation. Taken together, these data show a pivotal role for WNT signalling in gastric homoeostasis, FGP formation and adenomagenesis. Loss of the parietal cell population and corresponding FGP formation, an early event in gastric carcinogenesis, as well as antral adenoma formation are immediate effects of nuclear β-catenin translocation and WNT target gene expression. Furthermore, our inducible murine model will permit a better understanding of the molecular changes required to drive tumourigenesis in the stomach.

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Wnt Signaling in Renal Cancer

Cited by 41 publications

References 106 publications

Genomic Characterization of Gene Copy-Number Aberrations in Endometrial Carcinoma Cell Lines Derived from Endometrioid-Type Endometrial Adenocarcinoma

Genomic Characterization of Gene Copy-Number Aberrations in Endometrial Carcinoma Cell Lines Derived from Endometrioid-Type Endometrial Adenocarcinoma

VHL loss of function and its impact on oncogenic signaling networks in clear cell renal cell carcinoma

Acute WNT signalling activation perturbs differentiation within the adult stomach and rapidly leads to tumour formation

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