FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4290802308> ?p ?o ?g. }

• W4290802308 abstract "Background Ferroptosis plays an important role in the development of acute myeloid leukemia (AML); however, the exact role of ferroptosis-related genes in the prognosis of AML patients is unclear. Methods RNA sequencing data and the clinicopathological characteristics of AML patients were obtained from The Cancer Genome Atlas database, and ferroptosis-related genes were obtained from the FerrDb database. Cox regression analysis and least absolute shrinkage and selection operator analysis were performed to identify ferroptosis-related gene signatures. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and single-sample gene set enrichment analysis (ssGSEA) were performed to explore the biological functions of the ferroptosis-related genes. Finally, ferroptosis of AML cells was induced by erastin and sulfasalazine to detect the changes in the expression of relevant prognostic genes and explore the underlying mechanisms using quantitative real-time polymerase chain reaction (qRT-PCR). Results Seven ferroptosis-related gene signatures ( SOCS1 , ACSF2 , MYB , EIF2AK4 , AIFM2 , SLC7A11 , and GPX4 ) were identified in the training group. Kaplan-Meier and Cox regression analyses confirmed that risk score was an independent prognostic predictor of AML in the training and validation groups ( P &lt;0.05). Further, functional enrichment analysis revealed that seven ferroptosis-related genes were associated with many immune-related biological processes. Most importantly, erastin and sulfasalazine can induce the ferroptosis of AML cells. Overall, SLC7A11 and the SLC7A11/xCT-GSH-GPX4 pathway may be the respective key gene and potential regulatory pathway in erastin- and sulfasalazine-induced ferroptosis of AML cells. Conclusions A novel signature involving seven ferroptosis-related genes that could accurately predict AML prognosis was identified. Further, the Food and Drug Administration-approved drug, sulfasalazine, was demonstrated for the first time to induce the ferroptosis of AML cells. SLC7A11 and the SLC7A11/xCT-GSH-GPX4 pathway may be the respective key gene and underlying mechanism in this process, ultimately providing new insights into the strategies for the development of new AML therapies." @default.
• W4290802308 created "2022-08-12" @default.
• W4290802308 creator A5016768773 @default.
• W4290802308 creator A5032528396 @default.
• W4290802308 creator A5044205235 @default.
• W4290802308 creator A5044664499 @default.
• W4290802308 creator A5051444266 @default.
• W4290802308 creator A5052691524 @default.
• W4290802308 creator A5056995496 @default.
• W4290802308 creator A5058252911 @default.
• W4290802308 creator A5090123986 @default.
• W4290802308 date "2022-08-11" @default.
• W4290802308 modified "2023-10-05" @default.
• W4290802308 title "Comprehensive analysis of ferroptosis-related gene signatures as a potential therapeutic target for acute myeloid leukemia: A bioinformatics analysis and experimental verification" @default.
• W4290802308 cites W1997183854 @default.
• W4290802308 cites W2002490399 @default.
• W4290802308 cites W2028433016 @default.
• W4290802308 cites W2159707944 @default.
• W4290802308 cites W2165129832 @default.
• W4290802308 cites W2741315569 @default.
• W4290802308 cites W2762087180 @default.
• W4290802308 cites W2765817339 @default.
• W4290802308 cites W2770434260 @default.
• W4290802308 cites W2778627538 @default.
• W4290802308 cites W2807334922 @default.
• W4290802308 cites W2883979293 @default.
• W4290802308 cites W2904457678 @default.
• W4290802308 cites W2924471609 @default.
• W4290802308 cites W2964268954 @default.
• W4290802308 cites W2980472864 @default.
• W4290802308 cites W3000515035 @default.
• W4290802308 cites W3010133957 @default.
• W4290802308 cites W3012295934 @default.
• W4290802308 cites W3013967177 @default.
• W4290802308 cites W3022210151 @default.
• W4290802308 cites W3036293826 @default.
• W4290802308 cites W3090693089 @default.
• W4290802308 cites W3103771844 @default.
• W4290802308 cites W3110545125 @default.
• W4290802308 cites W3122102409 @default.
• W4290802308 cites W3123922203 @default.
• W4290802308 cites W3134122367 @default.
• W4290802308 cites W3138409534 @default.
• W4290802308 cites W3162306949 @default.
• W4290802308 cites W3180684760 @default.
• W4290802308 cites W3196858806 @default.
• W4290802308 cites W3208500726 @default.
• W4290802308 cites W3217558819 @default.
• W4290802308 cites W4200377209 @default.
• W4290802308 cites W4206460957 @default.
• W4290802308 cites W4210903129 @default.
• W4290802308 cites W4214889728 @default.
• W4290802308 cites W4221112683 @default.
• W4290802308 cites W4223490199 @default.
• W4290802308 doi "https://doi.org/10.3389/fonc.2022.930654" @default.
• W4290802308 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36033479" @default.
• W4290802308 hasPublicationYear "2022" @default.
• W4290802308 type Work @default.
• W4290802308 citedByCount "7" @default.
• W4290802308 countsByYear W42908023082022 @default.
• W4290802308 countsByYear W42908023082023 @default.
• W4290802308 crossrefType "journal-article" @default.
• W4290802308 hasAuthorship W4290802308A5016768773 @default.
• W4290802308 hasAuthorship W4290802308A5032528396 @default.
• W4290802308 hasAuthorship W4290802308A5044205235 @default.
• W4290802308 hasAuthorship W4290802308A5044664499 @default.
• W4290802308 hasAuthorship W4290802308A5051444266 @default.
• W4290802308 hasAuthorship W4290802308A5052691524 @default.
• W4290802308 hasAuthorship W4290802308A5056995496 @default.
• W4290802308 hasAuthorship W4290802308A5058252911 @default.
• W4290802308 hasAuthorship W4290802308A5090123986 @default.
• W4290802308 hasBestOaLocation W42908023081 @default.
• W4290802308 hasConcept C104317684 @default.
• W4290802308 hasConcept C150194340 @default.
• W4290802308 hasConcept C152724338 @default.
• W4290802308 hasConcept C162317418 @default.
• W4290802308 hasConcept C2778729363 @default.
• W4290802308 hasConcept C502942594 @default.
• W4290802308 hasConcept C54355233 @default.
• W4290802308 hasConcept C70721500 @default.
• W4290802308 hasConcept C86803240 @default.
• W4290802308 hasConceptScore W4290802308C104317684 @default.
• W4290802308 hasConceptScore W4290802308C150194340 @default.
• W4290802308 hasConceptScore W4290802308C152724338 @default.
• W4290802308 hasConceptScore W4290802308C162317418 @default.
• W4290802308 hasConceptScore W4290802308C2778729363 @default.
• W4290802308 hasConceptScore W4290802308C502942594 @default.
• W4290802308 hasConceptScore W4290802308C54355233 @default.
• W4290802308 hasConceptScore W4290802308C70721500 @default.
• W4290802308 hasConceptScore W4290802308C86803240 @default.
• W4290802308 hasFunder F4320321001 @default.
• W4290802308 hasFunder F4320328113 @default.
• W4290802308 hasLocation W42908023081 @default.
• W4290802308 hasLocation W42908023082 @default.
• W4290802308 hasLocation W42908023083 @default.
• W4290802308 hasLocation W42908023084 @default.
• W4290802308 hasOpenAccess W4290802308 @default.
• W4290802308 hasPrimaryLocation W42908023081 @default.
• W4290802308 hasRelatedWork W2009966535 @default.
• W4290802308 hasRelatedWork W2019988726 @default.

• next