FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3209576790> ?p ?o ?g. }

• W3209576790 abstract "Abstract Background Increased expression of the transcription factor Forkhead box M1 (FOXM1) has been reported to play an important role in the progression and development of multiple tumors, but the molecular mechanisms that regulate FOXM1 expression remain unknown, and the role of FOXM1 in aerobic glycolysis is still not clear. Methods The expression of FOXM1 and NADPH oxidase 4 (NOX4) in normal brain tissues and glioma was detected in data from the TCGA database and in our specimens. The effect of NOX4 on the expression of FOXM1 was determined by Western blot, qPCR, reactive oxygen species (ROS) production assays, and luciferase assays. The functions of NOX4 and FOXM1 in aerobic glycolysis in glioblastoma cells were determined by a series of experiments, such as Western blot, extracellular acidification rate (ECAR), lactate production, and intracellular ATP level assays. A xenograft mouse model was established to test our findings in vivo. Results The expression of FOXM1 and NOX4 was increased in glioma specimens compared with normal brain tissues and correlated with poor clinical outcomes. Aberrant mitochondrial reactive oxygen species (ROS) generation of NOX4 induced FOXM1 expression. Mechanistic studies demonstrated that NOX4-derived MitoROS exert their regulatory role on FOXM1 by mediating hypoxia-inducible factor 1α (HIF-1α) stabilization. Further research showed that NOX4-derived MitoROS-induced HIF-1α directly activates the transcription of FOXM1 and results in increased FOXM1 expression. Overexpression of NOX4 or FOXM1 promoted aerobic glycolysis, whereas knockdown of NOX4 or FOXM1 significantly suppressed aerobic glycolysis, in glioblastoma cells. NOX4-induced aerobic glycolysis was dependent on elevated FOXM1 expression, as FOXM1 knockdown abolished NOX4-induced aerobic glycolysis in glioblastoma cells both in vitro and in vivo. Conclusion Increased expression of FOXM1 induced by NOX4-derived MitoROS plays a pivotal role in aerobic glycolysis, and our findings suggest that inhibition of NOX4-FOXM1 signaling may present a potential therapeutic target for glioblastoma treatment." @default.
• W3209576790 created "2021-11-08" @default.
• W3209576790 creator A5006397303 @default.
• W3209576790 creator A5022717988 @default.
• W3209576790 creator A5026464336 @default.
• W3209576790 creator A5033702023 @default.
• W3209576790 creator A5035671110 @default.
• W3209576790 creator A5039225458 @default.
• W3209576790 creator A5044290349 @default.
• W3209576790 creator A5060396046 @default.
• W3209576790 creator A5063743958 @default.
• W3209576790 creator A5069149722 @default.
• W3209576790 date "2021-11-05" @default.
• W3209576790 modified "2023-10-16" @default.
• W3209576790 title "NOX4-derived ROS-induced overexpression of FOXM1 regulates aerobic glycolysis in glioblastoma" @default.
• W3209576790 cites W1550838463 @default.
• W3209576790 cites W1873822182 @default.
• W3209576790 cites W1962532958 @default.
• W3209576790 cites W2095987251 @default.
• W3209576790 cites W2117692326 @default.
• W3209576790 cites W2122816851 @default.
• W3209576790 cites W2129824771 @default.
• W3209576790 cites W2131668351 @default.
• W3209576790 cites W2157177585 @default.
• W3209576790 cites W2162868196 @default.
• W3209576790 cites W2163569233 @default.
• W3209576790 cites W2171293990 @default.
• W3209576790 cites W2212334442 @default.
• W3209576790 cites W2291628201 @default.
• W3209576790 cites W2544689467 @default.
• W3209576790 cites W2552872119 @default.
• W3209576790 cites W2575532686 @default.
• W3209576790 cites W2587281793 @default.
• W3209576790 cites W2619678328 @default.
• W3209576790 cites W2621333085 @default.
• W3209576790 cites W2752259410 @default.
• W3209576790 cites W2800247717 @default.
• W3209576790 cites W2804783721 @default.
• W3209576790 cites W2946948547 @default.
• W3209576790 cites W2969950932 @default.
• W3209576790 cites W2999903516 @default.
• W3209576790 cites W3012444409 @default.
• W3209576790 cites W3031224726 @default.
• W3209576790 cites W3033126715 @default.
• W3209576790 cites W3176225422 @default.
• W3209576790 doi "https://doi.org/10.1186/s12885-021-08933-y" @default.
• W3209576790 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8571893" @default.
• W3209576790 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34740322" @default.
• W3209576790 hasPublicationYear "2021" @default.
• W3209576790 type Work @default.
• W3209576790 sameAs 3209576790 @default.
• W3209576790 citedByCount "17" @default.
• W3209576790 countsByYear W32095767902022 @default.
• W3209576790 countsByYear W32095767902023 @default.
• W3209576790 crossrefType "journal-article" @default.
• W3209576790 hasAuthorship W3209576790A5006397303 @default.
• W3209576790 hasAuthorship W3209576790A5022717988 @default.
• W3209576790 hasAuthorship W3209576790A5026464336 @default.
• W3209576790 hasAuthorship W3209576790A5033702023 @default.
• W3209576790 hasAuthorship W3209576790A5035671110 @default.
• W3209576790 hasAuthorship W3209576790A5039225458 @default.
• W3209576790 hasAuthorship W3209576790A5044290349 @default.
• W3209576790 hasAuthorship W3209576790A5060396046 @default.
• W3209576790 hasAuthorship W3209576790A5063743958 @default.
• W3209576790 hasAuthorship W3209576790A5069149722 @default.
• W3209576790 hasBestOaLocation W32095767901 @default.
• W3209576790 hasConcept C104317684 @default.
• W3209576790 hasConcept C170240278 @default.
• W3209576790 hasConcept C173396325 @default.
• W3209576790 hasConcept C185592680 @default.
• W3209576790 hasConcept C20251656 @default.
• W3209576790 hasConcept C2779719074 @default.
• W3209576790 hasConcept C2779765511 @default.
• W3209576790 hasConcept C48349386 @default.
• W3209576790 hasConcept C502942594 @default.
• W3209576790 hasConcept C55493867 @default.
• W3209576790 hasConcept C55885012 @default.
• W3209576790 hasConcept C62231903 @default.
• W3209576790 hasConcept C86339819 @default.
• W3209576790 hasConcept C86803240 @default.
• W3209576790 hasConcept C95444343 @default.
• W3209576790 hasConceptScore W3209576790C104317684 @default.
• W3209576790 hasConceptScore W3209576790C170240278 @default.
• W3209576790 hasConceptScore W3209576790C173396325 @default.
• W3209576790 hasConceptScore W3209576790C185592680 @default.
• W3209576790 hasConceptScore W3209576790C20251656 @default.
• W3209576790 hasConceptScore W3209576790C2779719074 @default.
• W3209576790 hasConceptScore W3209576790C2779765511 @default.
• W3209576790 hasConceptScore W3209576790C48349386 @default.
• W3209576790 hasConceptScore W3209576790C502942594 @default.
• W3209576790 hasConceptScore W3209576790C55493867 @default.
• W3209576790 hasConceptScore W3209576790C55885012 @default.
• W3209576790 hasConceptScore W3209576790C62231903 @default.
• W3209576790 hasConceptScore W3209576790C86339819 @default.
• W3209576790 hasConceptScore W3209576790C86803240 @default.
• W3209576790 hasConceptScore W3209576790C95444343 @default.
• W3209576790 hasIssue "1" @default.
• W3209576790 hasLocation W32095767901 @default.
• W3209576790 hasLocation W32095767902 @default.
• W3209576790 hasLocation W32095767903 @default.

• next