<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Navarro P</submitter><funding>NLM NIH HHS</funding><funding>Department of Defense</funding><pagination>2604-15</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3645290</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>318(20)</volume><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</pubmed_abstract><journal>Experimental cell research</journal><pubmed_title>An indirect role for oncomir-519b in the expression of truncated neurokinin-1 in breast cancer cells.</pubmed_title><pmcid>PMC3645290</pmcid><funding_grant_id>#W81XWH-10-1-0413</funding_grant_id><funding_grant_id>T15 LM007092</funding_grant_id><pubmed_authors>Murthy RG</pubmed_authors><pubmed_authors>Rameshwar P</pubmed_authors><pubmed_authors>Shah S</pubmed_authors><pubmed_authors>Greco SJ</pubmed_authors><pubmed_authors>Park JM</pubmed_authors><pubmed_authors>Patel SA</pubmed_authors><pubmed_authors>Ramkissoon SH</pubmed_authors><pubmed_authors>Navarro P</pubmed_authors></additional><is_claimable>false</is_claimable><name>An indirect role for oncomir-519b in the expression of truncated neurokinin-1 in breast cancer cells.</name><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</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Dec</publication><modification>2026-04-16T21:23:59.928Z</modification><creation>2019-03-27T01:09:34Z</creation></dates><accession>S-EPMC3645290</accession><cross_references><pubmed>22981979</pubmed><doi>10.1016/j.yexcr.2012.09.002</doi></cross_references></HashMap>