FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2009715554> ?p ?o ?g. }

• W2009715554 endingPage "990" @default.
• W2009715554 startingPage "990" @default.
• W2009715554 abstract "Abstract CD82/KAI1 was one of the first metastasis suppressors identified and is capable of inhibiting the metastatic process in orthotopic tumor models. The expression of the CD82/KAI1 is down-regulated during tumor progression in many tumor types including prostate, breast, lung, bladder, and pancreatic cancers, and this down regulation appears to be at the level of transcription or post-transcription. The gene is not mutated, deleted or silenced by promoter methylation. CD82/KAI1 is also down regulated in advanced gynecologic cancers where CD82/KAI1 loss is associated with the poor overall survival in ovarian cancer. The mechanisms controlling the level of CD82/KAI1 expression remains unclear particularly the widespread loss in advanced cancers. The p53 tumor suppressor (TP53) can directly activate the CD82/KAI1 gene by interacting with the 5-prime upstream region of the CD82/KAI1 gene. Mutant TP53 is unable to bind this promoter site and fails to support CD82/KAI1 transcription. Taken together these data support a direct relationship between TP53 and CD82/KAI1 genes and suggested that the loss of TP53 function, which is common in many types of advanced cancer can lead to downregulation of CD82/KAI1, which then may result in metastases. However many cancers without TP53 mutation also exhibit loss of CD82/KAI1 suggesting that the mechanism for CD82/KAI1 loss is not completely explained by mutant TP53. Furthermore the mutant TP53 state and CD82/KAI1 loss is not strongly correlated in ovarian cancer. In some sarcomas the mechanism of CD82/KAI1 loss is related to the increase of the gp-78 E3 ligase and increased proteasomal degradation. Therefore the regulation of CD82/KAI1 in cells is likely complex. The AT Rich DNA binding protein ARID1A gene is frequently mutated in endometrial and ovarian cancers. In order to explore the functions of ARID1A in these cancers we complemented mutant ARID1A in the ACI-98 endometrial cancer cell line. We utilized a doxycycline inducible system and catalogued the protein changes following ARID1A complementation using LC MS/MS. Among the most differentially expressed proteins was CD82/KAI1. Levels of CD82 were dramatically increased following ARID1A induction. ACI-98 cells were found to be TP53 wild-type and CD82 expression null. QRT-PCR assays confirmed the dramatic increase in CD82/KAI1 mRNA levels and western blots also confirmed restoration of CD82/KAI1 protein following Doxycycline induced ARID1A restoration. We performed ChIP and confirmed that ARID1A was bound to the CD82/KAI1 promoter region close to the TP53 interaction area. Interestingly ACI-98 cells are mutant in both ARID1 homologs A and B. Ectopic expression of ARID1B was also able to restore expression of CD82/KAI1. These data suggest that the SWI/SNFARID1A/B complex is necessary for chromatin remodeling and expression of the CD82/KAI1 gene. Citation Format: Rusheeswar Challa, Yutaka Shoji, Kelly A. Conrads, Brian L. Hood, Guisong Wang, Kathleen M. Darcy, Chad A. Hamilton, George Larry Maxwell, Thomas P. Conrads, John I. Risinger. Metastasis suppressor CD82/KAI1 expression is dependent on functional SWI/SNF ARID1A/B. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 990. doi:10.1158/1538-7445.AM2014-990" @default.
• W2009715554 created "2016-06-24" @default.
• W2009715554 creator A5000738137 @default.
• W2009715554 creator A5003841051 @default.
• W2009715554 creator A5010088272 @default.
• W2009715554 creator A5032255820 @default.
• W2009715554 creator A5060699409 @default.
• W2009715554 creator A5080595928 @default.
• W2009715554 creator A5085457452 @default.
• W2009715554 creator A5089299085 @default.
• W2009715554 creator A5089660949 @default.
• W2009715554 creator A5090368690 @default.
• W2009715554 date "2014-10-01" @default.
• W2009715554 modified "2023-09-25" @default.
• W2009715554 title "Abstract 990: Metastasis suppressor CD82/KAI1 expression is dependent on functional SWI/SNF ARID1A/B" @default.
• W2009715554 doi "https://doi.org/10.1158/1538-7445.am2014-990" @default.
• W2009715554 hasPublicationYear "2014" @default.
• W2009715554 type Work @default.
• W2009715554 sameAs 2009715554 @default.
• W2009715554 citedByCount "1" @default.
• W2009715554 countsByYear W20097155542021 @default.
• W2009715554 crossrefType "journal-article" @default.
• W2009715554 hasAuthorship W2009715554A5000738137 @default.
• W2009715554 hasAuthorship W2009715554A5003841051 @default.
• W2009715554 hasAuthorship W2009715554A5010088272 @default.
• W2009715554 hasAuthorship W2009715554A5032255820 @default.
• W2009715554 hasAuthorship W2009715554A5060699409 @default.
• W2009715554 hasAuthorship W2009715554A5080595928 @default.
• W2009715554 hasAuthorship W2009715554A5085457452 @default.
• W2009715554 hasAuthorship W2009715554A5089299085 @default.
• W2009715554 hasAuthorship W2009715554A5089660949 @default.
• W2009715554 hasAuthorship W2009715554A5090368690 @default.
• W2009715554 hasConcept C121608353 @default.
• W2009715554 hasConcept C2778025950 @default.
• W2009715554 hasConcept C2778264664 @default.
• W2009715554 hasConcept C2779013556 @default.
• W2009715554 hasConcept C2909960190 @default.
• W2009715554 hasConcept C502942594 @default.
• W2009715554 hasConcept C54355233 @default.
• W2009715554 hasConcept C555283112 @default.
• W2009715554 hasConcept C86803240 @default.
• W2009715554 hasConceptScore W2009715554C121608353 @default.
• W2009715554 hasConceptScore W2009715554C2778025950 @default.
• W2009715554 hasConceptScore W2009715554C2778264664 @default.
• W2009715554 hasConceptScore W2009715554C2779013556 @default.
• W2009715554 hasConceptScore W2009715554C2909960190 @default.
• W2009715554 hasConceptScore W2009715554C502942594 @default.
• W2009715554 hasConceptScore W2009715554C54355233 @default.
• W2009715554 hasConceptScore W2009715554C555283112 @default.
• W2009715554 hasConceptScore W2009715554C86803240 @default.
• W2009715554 hasIssue "19_Supplement" @default.
• W2009715554 hasLocation W20097155541 @default.
• W2009715554 hasOpenAccess W2009715554 @default.
• W2009715554 hasPrimaryLocation W20097155541 @default.
• W2009715554 hasRelatedWork W1971774898 @default.
• W2009715554 hasRelatedWork W2002403933 @default.
• W2009715554 hasRelatedWork W2071141495 @default.
• W2009715554 hasRelatedWork W2085659118 @default.
• W2009715554 hasRelatedWork W2126934083 @default.
• W2009715554 hasRelatedWork W2363344444 @default.
• W2009715554 hasRelatedWork W24337117 @default.
• W2009715554 hasRelatedWork W4306156633 @default.
• W2009715554 hasRelatedWork W74547189 @default.
• W2009715554 hasRelatedWork W2163763011 @default.
• W2009715554 hasVolume "74" @default.
• W2009715554 isParatext "false" @default.
• W2009715554 isRetracted "false" @default.
• W2009715554 magId "2009715554" @default.
• W2009715554 workType "article" @default.