{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Navarro P"],"funding":["NLM NIH HHS","Department of Defense"],"pagination":["2604-15"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3645290"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["318(20)"],"pubmed_abstract":["Neurokinin 1 (NK1) encodes full-length (NK1-FL) and truncated (NK1-Tr) receptors, with distinct 3' UTR. NK1-Tr exerts oncogenic functions and is increased in breast cancer (BC). Enhanced transcription of NK1 resulted in higher level of NK1-Tr. The 3' UTR of these two transcripts are distinct with NK1-Tr terminating at a premature stop codon. NK1-Tr mRNA gained an advantage over NK1-FL with regards to translation. This is due to the ability of miR519B to interact with sequences within the 3' UTR of NK1-FL, but not NK1-Tr since the corresponding region is omitted. MiR519b suppressed the translation of NK1-FL in T47D and MDA-MB-231 resulting in increased NK1-Tr protein. Cytokines can induce the transcription of NK1. However, our studies indicated that translation appeared to be independent of"],"journal":["Experimental cell research"],"pubmed_title":["An indirect role for oncomir-519b in the expression of truncated neurokinin-1 in breast cancer cells."],"pmcid":["PMC3645290"],"funding_grant_id":["#W81XWH-10-1-0413","T15 LM007092"],"pubmed_authors":["Murthy RG","Rameshwar P","Shah S","Greco SJ","Park JM","Patel SA","Ramkissoon SH","Navarro P"],"additional_accession":[]},"is_claimable":false,"name":"An indirect role for oncomir-519b in the expression of truncated neurokinin-1 in breast cancer cells.","description":"Neurokinin 1 (NK1) encodes full-length (NK1-FL) and truncated (NK1-Tr) receptors, with distinct 3' UTR. NK1-Tr exerts oncogenic functions and is increased in breast cancer (BC). Enhanced transcription of NK1 resulted in higher level of NK1-Tr. The 3' UTR of these two transcripts are distinct with NK1-Tr terminating at a premature stop codon. NK1-Tr mRNA gained an advantage over NK1-FL with regards to translation. This is due to the ability of miR519B to interact with sequences within the 3' UTR of NK1-FL, but not NK1-Tr since the corresponding region is omitted. MiR519b suppressed the translation of NK1-FL in T47D and MDA-MB-231 resulting in increased NK1-Tr protein. Cytokines can induce the transcription of NK1. However, our studies indicated that translation appeared to be independent of","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Dec","modification":"2026-04-16T21:23:59.928Z","creation":"2019-03-27T01:09:34Z"},"accession":"S-EPMC3645290","cross_references":{"pubmed":["22981979"],"doi":["10.1016/j.yexcr.2012.09.002"]}}