FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2033072912> ?p ?o ?g. }

• W2033072912 abstract "Background: Superoxide dismutase 1 (SOD1), the ubiquitously expressed and predominant superoxide dismutase, catalyzes the conversion of superoxide ions into hydrogen peroxide which will be further detoxified by catalase or glutathione peroxidase. The SOD1 gene has been reported to be over-expressed in human cancer cells, and targeting SOD1 has been proposed as a new strategy for cancer therapy. While the transcriptional regulation of the SOD1 gene has been well-characterized, the contribution of the SOD1 3′-UTR to SOD1 gene expression has not been previously examined in any model systems. Methods: The full length (325 bases) and different fragments of the SOD1 3′UTR were amplified from human cancer cells. Each of the amplified products was inserted into a pGL3-promoter reporter vector downstream of the luciferase cDNA. The reporter constructs were transfected into Panc-1 (pancreatic cancer), A2780 (ovarian cancer), and HepG2 (liver cancer) cells and luciferase activity was analyzed. The wild type pGL3-promoter vector and the antisense orientation of the SOD1 3′-UTR reporter construct served as controls. Luciferase mRNA stability was examined by reverse transcriptase real-time PCR. Western blot was performed to examine endogenous SOD1 protein expression levels. Results: The luciferase activity was 10 (HepG2) and 70 (A2780 and Panc-1) fold higher in cells transfected with the full-length SOD1 3′-UTR compared with those in control cells. The dramatically increased luciferase activity was likely attributed to enhanced luciferase mRNA stability as analyzed by real-time RT-PCR. Significantly reduced luciferase activities were found in cells transfected with the reporter constructs bearing different fragments of the SOD1 3′-UTR. Most noticeably, transfection with the reporter construct bearing a deletion of the first 200 bases of the SOD1 3′-UTR brought the reporter activity down to a level similar to that in controls. Further deletion analysis showed that the secondary structure of the SOD1 3′-UTR may also play a key role in SOD1 3′-UTR-mediated gene expression and the putative AU-rich elements are unlikely to confer the sustained SOD1 gene expression. Moreover, we found that the full-length SOD1 3′-UTR can serve as a decoy or competitor to attenuate endogenous SOD1 protein expression, indicating the involvement of trans-acting RNA binding factors in maintaining high expression of the SOD1 gene. Summary: The SOD1 3′-UTR maintains the high expression of the SOD1 gene in human cancer cells likely through increasing SOD1 mRNA stability. The interaction of the SOD1 3′-UTR with the trans-acting RNA binding proteins is required to maintain SOD1 gene expression. We are actively working on identifying these RNA binding proteins and their interacting cis-elements in the SOD1 3′-UTR in our model systems. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4194. doi:1538-7445.AM2012-4194" @default.
• W2033072912 created "2016-06-24" @default.
• W2033072912 creator A5017401077 @default.
• W2033072912 creator A5028331497 @default.
• W2033072912 creator A5043152157 @default.
• W2033072912 creator A5073455841 @default.
• W2033072912 creator A5082206594 @default.
• W2033072912 date "2012-04-15" @default.
• W2033072912 modified "2023-09-26" @default.
• W2033072912 title "Abstract 4194: The superoxide dismutase 1 (SOD1) 3′-UTR maintains high expression of the SOD1 gene in cancer cells" @default.
• W2033072912 doi "https://doi.org/10.1158/1538-7445.am2012-4194" @default.
• W2033072912 hasPublicationYear "2012" @default.
• W2033072912 type Work @default.
• W2033072912 sameAs 2033072912 @default.
• W2033072912 citedByCount "0" @default.
• W2033072912 crossrefType "proceedings-article" @default.
• W2033072912 hasAuthorship W2033072912A5017401077 @default.
• W2033072912 hasAuthorship W2033072912A5028331497 @default.
• W2033072912 hasAuthorship W2033072912A5043152157 @default.
• W2033072912 hasAuthorship W2033072912A5073455841 @default.
• W2033072912 hasAuthorship W2033072912A5082206594 @default.
• W2033072912 hasConcept C104317684 @default.
• W2033072912 hasConcept C105580179 @default.
• W2033072912 hasConcept C111335760 @default.
• W2033072912 hasConcept C150194340 @default.
• W2033072912 hasConcept C153911025 @default.
• W2033072912 hasConcept C161733203 @default.
• W2033072912 hasConcept C181199279 @default.
• W2033072912 hasConcept C185592680 @default.
• W2033072912 hasConcept C2775838275 @default.
• W2033072912 hasConcept C2777615887 @default.
• W2033072912 hasConcept C33161422 @default.
• W2033072912 hasConcept C40767141 @default.
• W2033072912 hasConcept C502942594 @default.
• W2033072912 hasConcept C54009773 @default.
• W2033072912 hasConcept C55493867 @default.
• W2033072912 hasConcept C86803240 @default.
• W2033072912 hasConcept C89604277 @default.
• W2033072912 hasConceptScore W2033072912C104317684 @default.
• W2033072912 hasConceptScore W2033072912C105580179 @default.
• W2033072912 hasConceptScore W2033072912C111335760 @default.
• W2033072912 hasConceptScore W2033072912C150194340 @default.
• W2033072912 hasConceptScore W2033072912C153911025 @default.
• W2033072912 hasConceptScore W2033072912C161733203 @default.
• W2033072912 hasConceptScore W2033072912C181199279 @default.
• W2033072912 hasConceptScore W2033072912C185592680 @default.
• W2033072912 hasConceptScore W2033072912C2775838275 @default.
• W2033072912 hasConceptScore W2033072912C2777615887 @default.
• W2033072912 hasConceptScore W2033072912C33161422 @default.
• W2033072912 hasConceptScore W2033072912C40767141 @default.
• W2033072912 hasConceptScore W2033072912C502942594 @default.
• W2033072912 hasConceptScore W2033072912C54009773 @default.
• W2033072912 hasConceptScore W2033072912C55493867 @default.
• W2033072912 hasConceptScore W2033072912C86803240 @default.
• W2033072912 hasConceptScore W2033072912C89604277 @default.
• W2033072912 hasLocation W20330729121 @default.
• W2033072912 hasOpenAccess W2033072912 @default.
• W2033072912 hasPrimaryLocation W20330729121 @default.
• W2033072912 hasRelatedWork W1513520602 @default.
• W2033072912 hasRelatedWork W1552433276 @default.
• W2033072912 hasRelatedWork W1977712571 @default.
• W2033072912 hasRelatedWork W2016582989 @default.
• W2033072912 hasRelatedWork W2025685156 @default.
• W2033072912 hasRelatedWork W2028607043 @default.
• W2033072912 hasRelatedWork W2034406277 @default.
• W2033072912 hasRelatedWork W2038824969 @default.
• W2033072912 hasRelatedWork W2043729832 @default.
• W2033072912 hasRelatedWork W2047869040 @default.
• W2033072912 hasRelatedWork W2058055671 @default.
• W2033072912 hasRelatedWork W2060084840 @default.
• W2033072912 hasRelatedWork W2062856692 @default.
• W2033072912 hasRelatedWork W2066092356 @default.
• W2033072912 hasRelatedWork W2066556485 @default.
• W2033072912 hasRelatedWork W2283079036 @default.
• W2033072912 hasRelatedWork W2330235947 @default.
• W2033072912 hasRelatedWork W2350726616 @default.
• W2033072912 hasRelatedWork W2364959773 @default.
• W2033072912 hasRelatedWork W2393403313 @default.
• W2033072912 isParatext "false" @default.
• W2033072912 isRetracted "false" @default.
• W2033072912 magId "2033072912" @default.
• W2033072912 workType "article" @default.