RESEARCH ARTICLE Role of the splicing factor

head and neck and colorectal cancers. Cisplatin (cis-diamine platinum (II) dichloride), the founding member of this class of agents, covalently binds to DNA and induces the formation of bulky DNA adducts consisting of intra-strand cross-links preferentially formed between adjacent guanine residues and, to a lower extent, inter-sion repair, and inter-strand cross-links are removed via nucleotide excision repair, translesion polymerase and homologous recombination. Cisplatin activates various signalling pathways that include the DNA damage re-sponse (DDR) and the PI3K-Akt pathways [1]. The DDR pathway detects and corrects DNA defects. However, when alterations are too numerous or too severe, cells are committed to death and eliminated. The DDR ma-chinery relies on the activity of three enzymes that belong to the phosphatidyl inositol-3 kinases (PI3K) family: DNA-protein kinase (DNA-PK), Ataxia and Telangectasia * Correspondence