{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hepburn LA"],"funding":["European Research Council"],"pagination":["23029-23046"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5955416"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(33)"],"pubmed_abstract":["We show that suppression of the spliceosome has potential for the treatment of cutaneous squamous cell carcinoma (cSCC). The small-molecule inhibitors of the spliceosome at the most advanced stage of development target the splicing factor SF3B1/SF3b155. The majority of cSCC cell lines are more sensitive than normal skin cells to death induced by the SF3B1 inhibitor pladienolide B. Knockdown of SF3B1 and a range of other splicing factors with diverse roles in the spliceosome can also selectively kill cSCC cells. We demonstrate that endogenous c-MYC participates in conferring sensitivity to spliceosome inhibition. c-MYC expression is elevated in cSCC lines and its knockdown reduces alterations in mRNA splicing and attenuates cell death caused by interference with the spliceosome. In addition"],"journal":["Oncotarget"],"pubmed_title":["Targeting the spliceosome for cutaneous squamous cell carcinoma therapy: a role for c-MYC and wild-type p53 in determining the degree of tumour selectivity."],"pmcid":["PMC5955416"],"funding_grant_id":["250170"],"pubmed_authors":["Boag G","McHugh A","Leigh IM","Saville MK","Fernandes K","Proby CM","Hepburn LA"],"additional_accession":[]},"is_claimable":false,"name":"Targeting the spliceosome for cutaneous squamous cell carcinoma therapy: a role for c-MYC and wild-type p53 in determining the degree of tumour selectivity.","description":"We show that suppression of the spliceosome has potential for the treatment of cutaneous squamous cell carcinoma (cSCC). The small-molecule inhibitors of the spliceosome at the most advanced stage of development target the splicing factor SF3B1/SF3b155. The majority of cSCC cell lines are more sensitive than normal skin cells to death induced by the SF3B1 inhibitor pladienolide B. Knockdown of SF3B1 and a range of other splicing factors with diverse roles in the spliceosome can also selectively kill cSCC cells. We demonstrate that endogenous c-MYC participates in conferring sensitivity to spliceosome inhibition. c-MYC expression is elevated in cSCC lines and its knockdown reduces alterations in mRNA splicing and attenuates cell death caused by interference with the spliceosome. In addition","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 May","modification":"2026-05-01T19:49:10.718Z","creation":"2019-03-26T23:39:10Z"},"accession":"S-EPMC5955416","cross_references":{"pubmed":["29796170"],"doi":["10.18632/oncotarget.25196"]}}