Title : Caffeine induces tumor cytotoxicity via the regulation of alternative splicing in subsets of cancer-associated genes.

Pub. Date : 2014 Feb

PMID : 24333670






6 Functional Relationships(s)
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1 The detailed mechanisms of caffeine in tumor suppression via tumor suppressor protein p53 remain unclear. Caffeine tumor protein p53 Homo sapiens
2 In this study, we investigated how caffeine modulated cell cycle arrest and apoptosis via the expression of various alternatively spliced p53 isoforms. Caffeine tumor protein p53 Homo sapiens
3 Caffeine reduced p53alpha expression and induced the expression of p53beta, which contains an alternatively spliced p53 C-terminus. Caffeine tumor protein p53 Homo sapiens
4 Caffeine reduced p53alpha expression and induced the expression of p53beta, which contains an alternatively spliced p53 C-terminus. Caffeine tumor protein p53 Homo sapiens
5 Serine/arginine-rich splicing factor 3 was a promising candidate for the serine/arginine-rich splicing factors responsible for the alternative splicing of p53 in response to caffeine treatment. Caffeine tumor protein p53 Homo sapiens
6 In addition to p53-dependent functions, multiple target genes of serine/arginine-rich splicing factor 3 suggest that caffeine can regulate epithelial-mesenchymal-transition and hypoxic conditions to inhibit the survival of tumor cells. Caffeine tumor protein p53 Homo sapiens