Thousands of loci in the human and mouse genomes give rise to circular RNA transcripts; at many of these loci, the predominant RNA isoform is a circle. Using an improved computational approach for circular RNA identification, we found widespread circular RNA expression in Drosophila melanogaster and estimate that in humans, circular RNA may account for 1% as many molecules as poly(A) RNA. Analysis of data from the ENCODE consortium revealed that the repertoire of genes expressing circular RNA, the ratio of circular to linear transcripts for each gene, and even the pattern of splice isoforms of circular RNAs from each gene were cell-type specific. These results suggest that biogenesis of circular RNA is an integral, conserved, and regulated feature of the gene expression program.

/pdf/cell-type-specific-features-of-circular-rna-expression-4ao4gawmcm.pdf

Cell-type specific features of circular RNA expression.

Patrick O Brown should also be listed as a corresponding author. His email address is pbrown@stanford.edu

Correction: Cell-Type Specific Features of Circular RNA Expression

Cellular and Molecular effects of Vitamin D on Carcinogenesis

Vitamin D deficiency and low calcium intake are considered risk factors for several cancers. Vitamin D, synthesized in the skin or ingested through the diet, is transformed through two hydroxylation steps to the active metabolite, 1α,25-dihydroxyvitamin D3 (1,25-D3). 25-hydroxylases in the liver are responsible for the first hydroxylation step. The ultimate activation is performed by the renal 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1), while the 1,25-dihydroxyvitamin D 24-hydroxylase (CYP24A1) in the kidneys degrades the active metabolite. These two renal vitamin D hydroxylases control the endocrine serum 1,25-D3 levels, and are responsible for maintaining mineral homeostasis. In addition, the active vitamin D hormone 1,25-D3 regulates cellular proliferation, differentiation, and apoptosis in multiple tissues in a paracrine/autocrine manner. Interestingly, it is the low serum level of the precursor 25- hydroxyvitamin D3 (25-D3) that predisposes to numerous cancers and other chronic diseases, and not the serum concentration of the active vitamin D hormone. The extra-renal autocrine/paracrine vitamin D system is able to synthesize and degrade locally the active 1,25- D3 necessary to maintain normal cell growth and to counteract mitogenic stimuli. Thus, vitamin D hydroxylases play a prominent role in this process. The present review describes the role of the vitamin D hydroxylases in cancer pathogenesis and the cross-talk between the extra-renal autocrine/paracrine vitamin D system and calcium in cancer prevention.

Role of Calcium, Vitamin D, and the Extrarenal Vitamin D Hydroxylases in Carcinogenesis

Alternative pre-mRNA splicing allows exons of pre-mRNA to be spliced in different arrangements to produce functionally distinct mRNAs. More than 95% of human genes encode splice isoforms, some of which exert antagonistic functions. Recent studies revealed that alterations of the splicing machinery can cause the development of neoplasms, and understanding the splicing machinery is crucial for developing novel therapeutic strategies for malignancies. Colorectal cancer patients need novel strategies not only to enhance the efficacy of the currently available agents but also to utilize newly identified therapeutic targets. This review summarizes the current knowledge about the splice isoforms of VEGFA, UGT1A, PXR, cyclin D1, BIRC5 (survivin), DPD, K-RAS, SOX9, SLC39A14 and other genes, which may be possible therapeutic targets for colorectal cancer. Among them, the VEGFA splice isoforms are classified into VEGFAxxx and VEGFAxxxb, which have proangiogenic and antiangiogenic properties, respectively; UGT1A is alternatively spliced into UGT1A1 and other isoforms, which are regulated by pregnane X receptor isoforms and undergo further splicing modifications. Recently, the splicing machinery has been extensively investigated and novel discoveries in this research field are being reported at a rapid pace. The information contained in this review also provides suggestions for how therapeutic strategies targeting alternative splicing can be further developed.

/pdf/splice-isoforms-as-therapeutic-targets-for-colorectal-cancer-4wzshaf1pf.pdf

Splice isoforms as therapeutic targets for colorectal cancer.

CYP24A1 splice variants--implications for the antitumorigenic actions of 1,25-(OH)2D3 in colorectal cancer.

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CYP24A1 splice variants--implications for the antitumorigenic actions of 1,25-(OH)2D3 in colorectal cancer.