ArticleJournal of experimental & clinical cancer research : CR2010
Loss of heterozygosity and SOSTDC1 in adult and pediatric renal tumors.
Article in Journal of experimental & clinical cancer research : CR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Genetic variation frequencies in Wilms' tumor: A meta-analysis and systematic review.Cancer science · 2016Pooled it
- MEOX2: a homeobox transcription factor with multifaceted biological functions and broad disease associations.Frontiers in cell and developmental biology · 2026Review
- Wilms' Tumor: A Review of Clinical Characteristics, Treatment Advances, and Research Opportunities.Medicina (Kaunas, Lithuania) · 2025Review
- SOSTDC1 Nuclear Translocation Facilitates BTIC Maintenance and CHD1-Mediated HR Repair to Promote Tumor Progression and Olaparib Resistance in TNBC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of Sostdc1 in skeletal biology and cancer.Frontiers in physiology · 2022Review
- E4BP4 promotes thyroid cancer proliferation by modulating iron homeostasis through repression of hepcidin.Cell death & disease · 2018Article
- Population-specific genetic modification of Huntington's disease in Venezuela.PLoS genetics · 2018Article
- Promoter DNA methylation analysis reveals a novel diagnostic CpG-based biomarker and RAB25 hypermethylation in clear cell renel cell carcinoma.Scientific reports · 2017Article
- Transcriptome profiling of cancer and normal tissues from cervical squamous cancer patients by deep sequencing.Molecular medicine reports · 2017Article
- Wnt Signaling in Renal Cell Carcinoma.Cancers · 2016Review
- SOSTDC1 is down-regulated in non-small cell lung cancer and contributes to cancer cell proliferation.Cell & bioscience · 2016Article
- Down-regulation of SOSTDC1 promotes thyroid cancer cell proliferation via regulating cyclin A2 and cyclin E2.Oncotarget · 2015Article
- Sost and its paralog Sostdc1 coordinate digit number in a Gli3-dependent manner.Developmental biology · 2013Article
- The complex roles of Wnt antagonists in RCC.Nature reviews. Urology · 2011Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDeletions within the short arm of chromosome 7 are observed in approximately 25% of adult and 10% of Wilms pediatric renal tumors. Within Wilms tumors, the region of interest has been delineated to a 2-Mb minimal region that includes ten known genes. Two of these ten candidate genes, SOSTDC1 and MEOX2, are particularly relevant to tumor development and maintenance. This finding, coupled with evidence that SOSTDC1 is frequently downregulated in adult renal cancer and regulates both Wingless-Int (Wnt)- and bone morphogenetic protein (BMP)-induced signaling, points to a role for SOSTDC1 as a potential tumor suppressor.
methodsTo investigate this hypothesis, we interrogated the Oncomine database to examine the SOSTDC1 levels in adult renal clear cell tumors and pediatric Wilms tumors. We then performed single nucleotide polymorphism (SNP) and sequencing analyses of SOSTDC1 in 25 pediatric and 36 adult renal tumors. Immunohistochemical staining of patient samples was utilized to examine the impact of SOSTDC1 genetic aberrations on SOSTDC1 protein levels and signaling.
resultsWithin the Oncomine database, we found that SOSTDC1 levels were reduced in adult renal clear cell tumors and pediatric Wilms tumors. Through SNP and sequencing analyses of 25 Wilms tumors, we identified four with loss of heterozygosity (LOH) at 7p and three that affected SOSTDC1. Of 36 adult renal cancers, we found five with LOH at 7p, two of which affected SOSTDC1. Immunohistochemical analysis of SOSTDC1 protein levels within these tumors did not reveal a relationship between these instances of SOSTDC1 LOH and SOSTDC1 protein levels. Moreover, we could not discern any impact of these genetic alterations on Wnt signaling as measured by altered beta-catenin levels or localization.
conclusionsThis study shows that genetic aberrations near SOSTDC1 are not uncommon in renal cancer, and occur in adult as well as pediatric renal tumors. These observations of SOSTDC1 LOH, however, did not correspond with changes in SOSTDC1 protein levels or signaling regulation. Although our conclusions are limited by sample size, we suggest that an alternative mechanism such as epigenetic silencing of SOSTDC1 may be a key contributor to the reduced SOSTDC1 mRNA and protein levels observed in renal cancer.
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