Matches in SemOpenAlex for { <https://semopenalex.org/work/W4312447678> ?p ?o ?g. }
Showing items 1 to 70 of
70
with 100 items per page.
- W4312447678 abstract "Temozolomide (TMZ) resistance contributes to the unfavorable prognosis of glioma, however, the mechanism of resistance is unknown. ASK-1 has various functions in many tumors, but its function in glioma is poorly understood. This study aimed to elucidate the function of ASK-1 and the role of its modulators in the induction of TMZ resistance in glioma and the underlying mechanism.ASK-1 phosphorylation, the IC50 of TMZ, cell viability, and apoptosis were assessed in the U87 and U251 glioma cell lines and the derived TMZ-resistant cell lines U87-TR and U251-TR. We then blocked ASK-1 function, either with an inhibitor or by overexpression of multiple ASK-1 upstream modulators, to further explore the role of ASK-1 in TMZ-resistant glioma.TMZ-resistant glioma cells showed high IC50 values of TMZ, high survival, and low levels of apoptosis following the TMZ challenge. ASK-1 phosphorylation, but not protein expression, was higher in U87 and U251 cells than in TMZ-resistant glioma cells exposed to TMZ. The addition of the ASK-1 inhibitor selonsertib (SEL) resulted in the dephosphorylation of ASK-1 in U87 and U251 cells after the TMZ challenge. SEL treatment increased the TMZ resistance of U87 and U251 cells, as evidenced by the increased IC50 and cell survival rate and low apoptosis rate. Overexpression of some ASK-1 upstream suppressors [Thioredoxin (Trx), protein phosphatase 5 (PP5), 14-3-3, and cell division cycle 25C (Cdc25C)] led to various degrees of ASK-1 dephosphorylation and a TMZ-resistant phenotype in U87 and U251 cells.Dephosphorylation of ASK-1 induced TMZ resistance in human glioma cells, and several ASK-1 upstream suppressors, including Trx, PP5, 14-3-3, and Cdc25C, are involved in this phenotypic change induced by dephosphorylation of ASK-1." @default.
- W4312447678 created "2023-01-04" @default.
- W4312447678 creator A5002411548 @default.
- W4312447678 creator A5023831280 @default.
- W4312447678 creator A5029634246 @default.
- W4312447678 creator A5045029216 @default.
- W4312447678 creator A5051449882 @default.
- W4312447678 date "2022-01-01" @default.
- W4312447678 modified "2023-09-30" @default.
- W4312447678 title "Multiple pathway-dephosphorylated ask-1 confers temozolomide resistance to human glioma cells" @default.
- W4312447678 doi "https://doi.org/10.5137/1019-5149.jtn.41212-22.1" @default.
- W4312447678 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36951032" @default.
- W4312447678 hasPublicationYear "2022" @default.
- W4312447678 type Work @default.
- W4312447678 citedByCount "0" @default.
- W4312447678 crossrefType "journal-article" @default.
- W4312447678 hasAuthorship W4312447678A5002411548 @default.
- W4312447678 hasAuthorship W4312447678A5023831280 @default.
- W4312447678 hasAuthorship W4312447678A5029634246 @default.
- W4312447678 hasAuthorship W4312447678A5045029216 @default.
- W4312447678 hasAuthorship W4312447678A5051449882 @default.
- W4312447678 hasConcept C11960822 @default.
- W4312447678 hasConcept C128473837 @default.
- W4312447678 hasConcept C136264566 @default.
- W4312447678 hasConcept C162324750 @default.
- W4312447678 hasConcept C178666793 @default.
- W4312447678 hasConcept C181912034 @default.
- W4312447678 hasConcept C190283241 @default.
- W4312447678 hasConcept C2777389519 @default.
- W4312447678 hasConcept C2778227246 @default.
- W4312447678 hasConcept C29537977 @default.
- W4312447678 hasConcept C502942594 @default.
- W4312447678 hasConcept C55493867 @default.
- W4312447678 hasConcept C71924100 @default.
- W4312447678 hasConcept C86803240 @default.
- W4312447678 hasConcept C90329073 @default.
- W4312447678 hasConcept C95444343 @default.
- W4312447678 hasConceptScore W4312447678C11960822 @default.
- W4312447678 hasConceptScore W4312447678C128473837 @default.
- W4312447678 hasConceptScore W4312447678C136264566 @default.
- W4312447678 hasConceptScore W4312447678C162324750 @default.
- W4312447678 hasConceptScore W4312447678C178666793 @default.
- W4312447678 hasConceptScore W4312447678C181912034 @default.
- W4312447678 hasConceptScore W4312447678C190283241 @default.
- W4312447678 hasConceptScore W4312447678C2777389519 @default.
- W4312447678 hasConceptScore W4312447678C2778227246 @default.
- W4312447678 hasConceptScore W4312447678C29537977 @default.
- W4312447678 hasConceptScore W4312447678C502942594 @default.
- W4312447678 hasConceptScore W4312447678C55493867 @default.
- W4312447678 hasConceptScore W4312447678C71924100 @default.
- W4312447678 hasConceptScore W4312447678C86803240 @default.
- W4312447678 hasConceptScore W4312447678C90329073 @default.
- W4312447678 hasConceptScore W4312447678C95444343 @default.
- W4312447678 hasLocation W43124476781 @default.
- W4312447678 hasLocation W43124476782 @default.
- W4312447678 hasOpenAccess W4312447678 @default.
- W4312447678 hasPrimaryLocation W43124476781 @default.
- W4312447678 hasRelatedWork W2040830156 @default.
- W4312447678 hasRelatedWork W2070897281 @default.
- W4312447678 hasRelatedWork W2344922343 @default.
- W4312447678 hasRelatedWork W2560629363 @default.
- W4312447678 hasRelatedWork W2745825872 @default.
- W4312447678 hasRelatedWork W2888674289 @default.
- W4312447678 hasRelatedWork W2902070627 @default.
- W4312447678 hasRelatedWork W3005634848 @default.
- W4312447678 hasRelatedWork W3013154413 @default.
- W4312447678 hasRelatedWork W4220865729 @default.
- W4312447678 isParatext "false" @default.
- W4312447678 isRetracted "false" @default.
- W4312447678 workType "article" @default.