Biochemical and Biophysical Research Communications
Regular ArticleAlternative Splicing of CD44 pre-mRNA in Human Colorectal Tumors
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Discovery of novel transcripts of the human tissue kallikrein (KLK1) and kallikrein-related peptidase 2 (KLK2) in human cancer cells, exploiting Next-Generation Sequencing technology
2019, GenomicsCitation Excerpt :Alternative splicing of cancer-related genes has previously been shown to play important roles in cell cycle control, proliferation, apoptosis, angiogenesis, as well as invasion and metastasis [30]. In spite of the fact that the relationship between particular splicing events and the etiology of cancer is not yet fully understood, novel splice variants may constitute new, attractive molecular biomarkers that could be exploited for diagnostic and/or prognostic purposes, potential biomarkers for response or resistance to treatment, as well as therapeutic targets [31–37]. The family of KLKs constitutes a prominent example, as all its members have been shown to be subjected to intense alternative splicing.
Novel alternative splice variants of the human protein arginine methyltransferase 1 (PRMT1) gene, discovered using next-generation sequencing
2019, GeneCitation Excerpt :In fact, alternative splicing has a critical impact on many fundamental aspects of cell biology, including cell cycle control and apoptosis (Kim et al., 2008). Despite the fact that in most cases the relationship between a specific splicing event and the etiology of cancer is not yet fully understood, novel alternatively spliced transcripts could appear as new molecular biomarkers for diagnostic or prognostic purposes, and/or as potential targets for therapeutic strategies (Finn et al., 1994). Splicing patterns of several genes have been reported to be altered in cancers, including those encoding the prolactin receptor, RON receptor tyrosine kinase, the small signaling G protein RAC1, fibronectin, fibroblast growth factor receptors (FGFRs), CD44, and the MDM2 proto-oncogene.
Methylmercury exposure alters RNA splicing in human neuroblastoma SK-N-SH cells: Implications from proteomic and post-transcriptional responses
2018, Environmental PollutionCitation Excerpt :For example, the misregulation of alternative splicing of survival motor neuron 2 exon 7 was shown to cause spinal muscular atrophy, which is a common neurodegenerative disease (Kashima and Manley, 2003). Misregulation of several genes (CD44 and MUC2) was found to correlate with human colorectal tumors (Finn et al., 1994; Gardina et al., 2006; Sternberg et al., 2004). Numerous genomic, transcriptomic, and proteomic-based technologies were applied to assess the expression profiles of genes, RNAs, and proteins in response to heavy metal exposure using various tissues and cell lines.
Regulation of CD44 expression by tumor necrosis factor-α and its potential role in breast cancer cell migration
2012, Biomedicine and PharmacotherapyCitation Excerpt :Abnormal high level of CD44v6 is often present in advanced colorectal cancer, lung cancer and BC [13,23,24]. In tumor cells with enhanced migrating ability, abnormal high level of CD44v6 prevents tumor cells from the identification and killing of human immune system, resulting in lymph nodes involvement and distant metastasis [25,26]. Our study revealed that TNF-α could regulate CD44 expression in BC.
Gene expression changes reveal patterns of aging in the rat digestive tract
2005, Ageing Research ReviewsIdentification of sequence motifs responsible for the adhesive interaction between exon v10-containing CD44 isoforms
2002, Journal of Biological ChemistryCitation Excerpt :Finally, as expected, the low level binding of TILJhCD44R1 cells to COS cells expressing CD44R1.R288S was not further reduced by chondroitinase ABC treatment, strongly suggesting that it is the recognition of CS, mediated by the presence within exon v10 of an additional B[X 7]B motif, that is primarily responsible for the reciprocal adhesive interaction between exon v10-containing CD44 isoforms. Although previous studies have demonstrated a correlation between the expression of certain exon v10-containing CD44 isoforms and enhanced tumor metastasis and/or poor prognosis (1, 2, 4), the molecular mechanisms that underlie this important relationship have yet to be elucidated. Some initial experiments suggested that CD44H and CD44R1 may differ in their ability to bind the extracellular matrix glycosaminoglycan HA (19, 20).