FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4245398518> ?p ?o ?g. }

• W4245398518 endingPage "3432" @default.
• W4245398518 startingPage "3432" @default.
• W4245398518 abstract "Abstract Glioblastoma (GBM) is the most malignant brain cancer, with extremely poor prognosis in patients. GBM tumors are characterized by distinct molecular subtypes, known as proneural (PN), classical, and mesenchymal (MES). Inherited heterogeneity and aberrant aggressiveness contribute to therapy resistance and frequent recurrence of malignant GBM tumors. In addition, GBM tumors also contain a small subpopulation of tumor-initiating or stem-like cancer cells (GSCs). Gene expression profiling studies from our laboratory showed that patient-derived GSCs can also be classified into two subtypes, PN and MES, that are phenotypically similar to clinical GBM. Among three thousand genes that are differentially expressed between PN and MES-like GSCs, Lymphocyte Antigen 6 Complex, Locus K (LY6K) was identified as one of the top differentially expressed genes. LY6K is a GPI-anchored protein from the LY6 family. Several members of the LY6 family have been implicated in human cancers, including breast, esophageal, and lung cancers. Moreover, the function of LY6K in GBM has not been reported. Here, we examined the roles of LY6K upregulation in GBM tumorigenesis and investigated the underlying mechanism of LY6K action. We hypothesized that high levels of LY6K in GSCs promotes GBM tumorigenesis. Based on our other preliminary data, we further hypothesized that LY6K functions by enhancing ERK activation, thus promoting radioresistance. To test our hypotheses, we first examined the role of LY6K in advancing GBM tumorigenic behaviors of GSCs. We performed in vitro and in vivo tumorigenicity assays and showed that the presence of LY6K significantly increases GSC cell growth and glioma sphere forming ability in vitro and promotes tumor formation in orthotopic brain xenograft mouse models. The underlying mechanism governing LY6K expression was found to be DNA promoter methylation. Moreover, irradiation strongly induces LY6K expression via demethylation of LY6K promoter in GSCs with otherwise undetectable levels of LY6K. Furthermore, we investigated the mechanism by which LY6K contributes to GSC tumorigenicity. We observed that there is a strong relationship between LY6K and ERK signaling in GSCs and U87 glioma cells. The presence of LY6K stimulates ERK activation and subsequently augments cell proliferation of GSCs. Lastly, we identified the GPI-anchor domain of LY6K as a key region in enhancing ERK activation and are currently examining the mechanistic properties of this domain. The mechanistic insights gained from our studies will advance current knowledge of aberrantly upregulated LY6K and ERK signaling enhancement in promoting GBM tumorigenicity. Citation Format: Namratha G. Sastry, Tianzhi Huang, Angel Alvarez, Rajendra Pangeni, Xiao Song, Xuechao Wan, John Kessler, Ichiro Nakano, Bo Hu, Shi-Yuan Cheng. Novel roles of LY6K in glioblastoma tumorigenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 3432." @default.
• W4245398518 created "2022-05-12" @default.
• W4245398518 creator A5013074988 @default.
• W4245398518 creator A5020042371 @default.
• W4245398518 creator A5021857158 @default.
• W4245398518 creator A5023989141 @default.
• W4245398518 creator A5029832154 @default.
• W4245398518 creator A5037386621 @default.
• W4245398518 creator A5072854024 @default.
• W4245398518 creator A5077581859 @default.
• W4245398518 creator A5078890396 @default.
• W4245398518 creator A5080154231 @default.
• W4245398518 date "2019-07-01" @default.
• W4245398518 modified "2023-09-27" @default.
• W4245398518 title "Abstract 3432: Novel roles of LY6K in glioblastoma tumorigenesis" @default.
• W4245398518 doi "https://doi.org/10.1158/1538-7445.am2019-3432" @default.
• W4245398518 hasPublicationYear "2019" @default.
• W4245398518 type Work @default.
• W4245398518 citedByCount "0" @default.
• W4245398518 crossrefType "journal-article" @default.
• W4245398518 hasAuthorship W4245398518A5013074988 @default.
• W4245398518 hasAuthorship W4245398518A5020042371 @default.
• W4245398518 hasAuthorship W4245398518A5021857158 @default.
• W4245398518 hasAuthorship W4245398518A5023989141 @default.
• W4245398518 hasAuthorship W4245398518A5029832154 @default.
• W4245398518 hasAuthorship W4245398518A5037386621 @default.
• W4245398518 hasAuthorship W4245398518A5072854024 @default.
• W4245398518 hasAuthorship W4245398518A5077581859 @default.
• W4245398518 hasAuthorship W4245398518A5078890396 @default.
• W4245398518 hasAuthorship W4245398518A5080154231 @default.
• W4245398518 hasConcept C104317684 @default.
• W4245398518 hasConcept C121608353 @default.
• W4245398518 hasConcept C127561419 @default.
• W4245398518 hasConcept C142724271 @default.
• W4245398518 hasConcept C2776256026 @default.
• W4245398518 hasConcept C2777609662 @default.
• W4245398518 hasConcept C2778227246 @default.
• W4245398518 hasConcept C28328180 @default.
• W4245398518 hasConcept C502942594 @default.
• W4245398518 hasConcept C54355233 @default.
• W4245398518 hasConcept C555283112 @default.
• W4245398518 hasConcept C58962609 @default.
• W4245398518 hasConcept C62478195 @default.
• W4245398518 hasConcept C71924100 @default.
• W4245398518 hasConcept C81885089 @default.
• W4245398518 hasConcept C86554907 @default.
• W4245398518 hasConcept C86803240 @default.
• W4245398518 hasConceptScore W4245398518C104317684 @default.
• W4245398518 hasConceptScore W4245398518C121608353 @default.
• W4245398518 hasConceptScore W4245398518C127561419 @default.
• W4245398518 hasConceptScore W4245398518C142724271 @default.
• W4245398518 hasConceptScore W4245398518C2776256026 @default.
• W4245398518 hasConceptScore W4245398518C2777609662 @default.
• W4245398518 hasConceptScore W4245398518C2778227246 @default.
• W4245398518 hasConceptScore W4245398518C28328180 @default.
• W4245398518 hasConceptScore W4245398518C502942594 @default.
• W4245398518 hasConceptScore W4245398518C54355233 @default.
• W4245398518 hasConceptScore W4245398518C555283112 @default.
• W4245398518 hasConceptScore W4245398518C58962609 @default.
• W4245398518 hasConceptScore W4245398518C62478195 @default.
• W4245398518 hasConceptScore W4245398518C71924100 @default.
• W4245398518 hasConceptScore W4245398518C81885089 @default.
• W4245398518 hasConceptScore W4245398518C86554907 @default.
• W4245398518 hasConceptScore W4245398518C86803240 @default.
• W4245398518 hasIssue "13_Supplement" @default.
• W4245398518 hasLocation W42453985181 @default.
• W4245398518 hasOpenAccess W4245398518 @default.
• W4245398518 hasPrimaryLocation W42453985181 @default.
• W4245398518 hasRelatedWork W1981027541 @default.
• W4245398518 hasRelatedWork W2097372335 @default.
• W4245398518 hasRelatedWork W2148383305 @default.
• W4245398518 hasRelatedWork W2379132232 @default.
• W4245398518 hasRelatedWork W2543495975 @default.
• W4245398518 hasRelatedWork W2580196525 @default.
• W4245398518 hasRelatedWork W2740068052 @default.
• W4245398518 hasRelatedWork W3005421382 @default.
• W4245398518 hasRelatedWork W3022564264 @default.
• W4245398518 hasRelatedWork W3049714071 @default.
• W4245398518 hasVolume "79" @default.
• W4245398518 isParatext "false" @default.
• W4245398518 isRetracted "false" @default.
• W4245398518 workType "article" @default.