ArticleCarcinogenesis2010
Apc(MIN) modulation of vitamin D secosteroid growth control.
Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.Frontiers in genetics · 2024Review
- Vitamin D and Hypoxia: Points of Interplay in Cancer.Cancers · 2022Review
- Is Vitamin D Deficiency Related to Increased Cancer Risk in Patients with Type 2 Diabetes Mellitus?International journal of molecular sciences · 2021Review
- Wnt and Vitamin D at the Crossroads in Solid Cancer.Cancers · 2020Review
- Skeletal and Extraskeletal Actions of Vitamin D: Current Evidence and Outstanding Questions.Endocrine reviews · 2019Review
- Therapeutic Efficacy of Vitamin D in Experimental c-MET-β-Catenin-Driven Hepatocellular Cancer.Gene expression · 2019Article
- Extraskeletal actions of vitamin D.Annals of the New York Academy of Sciences · 2016Review
- Vitamin D and colorectal cancer: molecular, epidemiological and clinical evidence.The British journal of nutrition · 2016Review
- Vitamin D and the Epithelial to Mesenchymal Transition.Stem cells international · 2016Review
- Regulation of VDR Expression in Apc-Mutant Mice, Human Colon Cancers and Adenomas.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Targeting cancer stem cells in solid tumors by vitamin D.The Journal of steroid biochemistry and molecular biology · 2015Review
- The effect of 1,25 dihydroxyvitamin D3 treatment on the mRNA levels of β catenin target genes in mice with colonic inactivation of both APC alleles.The Journal of steroid biochemistry and molecular biology · 2015Review
- Vitamin D and colon cancer.World journal of gastrointestinal oncology · 2014Review
- Animal models of gastrointestinal and liver diseases. New mouse models for studying dietary prevention of colorectal cancer.American journal of physiology. Gastrointestinal and liver physiology · 2014Review
- Vitamin D and cancer: the promise not yet fulfilled.Endocrine · 2014Review
- Article
- Molecular link between vitamin D and cancer prevention.Nutrients · 2013Review
- Prevention of preneoplastic lesions by dietary vitamin D in a mouse model of colorectal carcinogenesis.The Journal of steroid biochemistry and molecular biology · 2013Article
- Importance of apical membrane delivery of 1,25-dihydroxyvitamin D3 to vitamin D-responsive gene expression in the colon.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Hepatic stem cells and transforming growth factor β in hepatocellular carcinoma.Nature reviews. Gastroenterology & hepatology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A central paradox of vitamin D biology is that 1alpha,25-(OH)(2) D(3) exposure inversely relates to colorectal cancer (CRC) risk despite a capacity for activation of both pro- and anti-oncogenic mediators including osteopontin (OPN)/CD44 and E-cadherin, respectively. Most sporadic CRCs arise from adenomatous polyposis coli (APC) gene mutation but understanding of its effects on vitamin D growth control is limited. Here we investigate effects of the Apc(Min/+) genotype on 1alpha,25-(OH)(2) D(3) regulation of OPN/CD44/E-cadherin signalling and intestinal tumourigenesis, in vivo. In untreated Apc(Min/+) versus Apc(+/+) intestines, expression levels of OPN and its CD44 receptor were increased, whereas E-cadherin tumour suppressor signalling was attenuated. Treatment by 1alpha,25-(OH)(2) D(3) or rationally designed analogues (QW or BTW) enhanced OPN but inhibited expression of CD44, the OPN receptor implicated in cell growth. These treatments also enhanced E-cadherin tumour suppressor activity, characterized by inhibition of beta-catenin nuclear localization, T-cell factor 1 and c-myelocytomatosis protein expression in Apc(Min/+) intestine. All secosteroids suppressed Apc(Min/+)-driven tumourigenesis although QW and BTW had lower calcium-related toxicity. Taken together, these data indicate that the Apc(Min/+) genotype modulates vitamin D secosteroid actions to promote functional predominance of E-cadherin tumour suppressor activity within antagonistic molecular networks. APC heterozygosity may promote favourable tissue- or tumour-specific conditions for growth control by vitamin D secosteroid treatment.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.