Expression of splice variants of 1α-hydroxylase in mcf-7 breast cancer cells

Cordes, T.; Diesing, D.; Becker, Steffi; Fischer, Dorothea; Diedrich, K.; Friedrich, Michael

doi:10.1016/j.jsbmb.2006.12.034

Cited by 14 publications

(10 citation statements)

References 21 publications

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“…However, clinical data on CYP27B1 expression in breast cancer is inconsistent (Segersten et al, 2005; Townsend et al, 2005; de Lyra et al, 2006; McCarthy et al, 2009; Lopes et al, 2010) and less than 2% of breast cancers annotated in The Cancer Genome Atlas datasets exhibit genomic alterations in CYP27B1. However, altered splice variants of CYP27B1 have been detected in breast cancer cells (Cordes et al, 2007; Fischer et al, 2007) suggesting the possibility that forms of the CYP27B1 enzyme with altered function could be expressed in breast tumors.…”

Section: Vitamin D Pathway Expression In Established Breast Cancermentioning

confidence: 99%

The impact of vitamin D in breast cancer: genomics, pathways, metabolism

et al. 2014

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Nuclear receptors exert profound effects on mammary gland physiology and have complex roles in the etiology of breast cancer. In addition to receptors for classic steroid hormones such as estrogen and progesterone, the nuclear vitamin D receptor (VDR) interacts with its ligand 1α,25(OH)2D3 to modulate the normal mammary epithelial cell genome and subsequent phenotype. Observational studies suggest that vitamin D deficiency is common in breast cancer patients and that low vitamin D status enhances the risk for disease development or progression. Genomic profiling has characterized many 1α,25(OH)2D3 responsive targets in normal mammary cells and in breast cancers, providing insight into the molecular actions of 1α,25(OH)2D3 and the VDR in regulation of cell cycle, apoptosis, and differentiation. New areas of emphasis include regulation of tumor metabolism and innate immune responses. However, the role of VDR in individual cell types (i.e., epithelial, adipose, fibroblast, endothelial, immune) of normal and tumor tissues remains to be clarified. Furthermore, the mechanisms by which VDR integrates signaling between diverse cell types and controls soluble signals and paracrine pathways in the tissue/tumor microenvironment remain to be defined. Model systems of carcinogenesis have provided evidence that both VDR expression and 1α,25(OH)2D3 actions change with transformation but clinical data regarding vitamin D responsiveness of established tumors is limited and inconclusive. Because breast cancer is heterogeneous, analysis of VDR actions in specific molecular subtypes of the disease may help to clarify the conflicting data. The expanded use of genomic, proteomic and metabolomic approaches on a diverse array of in vitro and in vivo model systems is clearly warranted to comprehensively understand the network of vitamin D regulated pathways in the context of breast cancer.

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Section: Vitamin D Pathway Expression In Established Breast Cancermentioning

confidence: 99%

The impact of vitamin D in breast cancer: genomics, pathways, metabolism

et al. 2014

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“…Fischer and co-workers [148] showed 6 different variants of the enzyme in MCF10F via nested touchdown PCR, but in MCF-7, these variants appeared weakly expressed. Based on this data, the authors concluded that because alternative splicing regulates the level of the active enzyme extrarenaly it therefore regulates the local production of 1,25(OH) 2 D 3 [149]. The activity of the extrarenally expressed 1-α-hydroxylase is an important factor of the tumor pathophysiology because of an accumulation of 1,25(OH) 2 D 3 in many tissues.…”

Section: Extrarenal Vitamin D Metabolizing Enzymesmentioning

confidence: 99%

1,25(OH)2D3 and Cyclooxygenase-2: Possible Targets for Breast Cancer?

Thill¹,

Becker²,

Fischer³

et al. 2011

Breast Cancer - Carcinogenesis, Cell Growth and Signalling Pathways

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“…Published reports have described splice variant mRNA transcripts for the vitamin D-activating enzyme 25-hydroxyvitamin D-1α-hydroxylase ( CYP27B1 ) [29–35]. Data from these studies have underlined a potential role for CYP27B1 splice variants in regulating localized synthesis of 1,25(OH) 2 D [32], notably in the context of tissue-specific regulation of this active from of vitamin D [31].…”

Section: Vitamin D and Rna Splicingmentioning

confidence: 99%

Vitamin D and alternative splicing of RNA

Zhou

Chun

Lisse

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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The active form of vitamin D (1α,25-dihydroxyvitamin D, 1,25(OH)2D) exerts its genomic effects via binding to a nuclear high-affinity vitamin D receptor (VDR). Recent deep sequencing analysis of VDR binding locations across the complete genome has significantly expanded our understanding of the actions of vitamin D and VDR on gene transcription. However, these studies have also promoted appreciation of the extra-transcriptional impact of vitamin D on gene expression. It is now clear that vitamin D interacts with the epigenome via effects on DNA methylation, histone acetylation, and microRNA generation to maintain normal biological functions. There is also increasing evidence that vitamin D can influence pre-mRNA constitutive splicing and alternative splicing, although the mechanism for this remains unclear. Pre-mRNA splicing has long been thought to be a post-transcription RNA processing event, but current data indicate that this occurs co-transcriptionally. Several steroid hormones have been recognized to coordinately control gene transcription and pre-mRNA splicing through the recruitment of nuclear receptor co-regulators that can both control gene transcription and splicing. The current review will discuss this concept with specific reference to vitamin D, and the potential role of heterogeneous nuclear ribonucleoprotein C (hnRNPC), a nuclear factor with an established function in RNA splicing. hnRNPC, has been shown to be involved in the VDR transcriptional complex as a vitamin D-response element-binding protein (VDRE-BP), and may act as a coupling factor linking VDR-directed gene transcription with RNA splicing. In this way hnRNPC may provide an additional mechanism for the fine-tuning of vitamin D-regulated target gene expression.

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Expression of splice variants of 1α-hydroxylase in mcf-7 breast cancer cells

Cited by 14 publications

References 21 publications

The impact of vitamin D in breast cancer: genomics, pathways, metabolism

The impact of vitamin D in breast cancer: genomics, pathways, metabolism

1,25(OH)2D3 and Cyclooxygenase-2: Possible Targets for Breast Cancer?

Vitamin D and alternative splicing of RNA

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