FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2892975930> ?p ?o ?g. }

• W2892975930 endingPage "6404" @default.
• W2892975930 startingPage "6395" @default.
• W2892975930 abstract "H19 induced by oxidative stress confers temozolomide resistance in human glioma cells via activating NF-κB signaling Shibo Duan,1,* Ming Li,2,* Zhifeng Wang,1 Longlong Wang,1 Yongjie Liu1 1Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei Province, People’s Republic of China; 2Department of Obstetrics, Cangzhou Central Hospital, Cangzhou, Hebei Province, People’s Republic of China *These authors contributed equally to this work Background: Recent findings around long noncoding RNAs (lncRNAs) have opened novel areas of research around their prospective use in overcoming chemoresistance. Herein, we aimed to investigate the role of lncRNA H19 in temozolomide (TMZ) resistance of human glioma cells and the possible mechanisms.Methods: Short-/long-term oxidative stress was induced, and TMZ-resistant glioma cells (U251TMZ and LN229TMZ) were established. Small interfering RNA (siRNA) and overexpression plasmids were used to modulate the expression of H19 and/or luciferase the reporters. The MTT assay and immunoblotting of cleaved caspase-3, cyclin D1, XIAP and Bcl-2 were conducted to evaluate TMZ sensitivity. Luciferase reporter and quantitative real-time PCR (qRT-PCR) assays were used to verify the activation of NF-κB pathways by H19.Results: Knockdown of H19 in U251TMZ and LN229TMZ cells decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis, and H19 overexpression in U251 and LN229 cells led to the opposite effects, indicating that the H19 confers TMZ resistance to glioma cells. Furthermore, knockdown of H19 decreased the NF-κB signaling, which was revealed by repressed reporter activity and declined expression of its downstream targets in TMZ-resistant glioma cells. In contrast, H19 overexpression in U251 and LN229 cells resulted in an increase in NF-κB activation. Blockage of NF-κB activation by its inhibitor abolished TMZ resistance caused by H19 overexpression. Addition of H2O2 to induce oxidative stress largely reversed TMZ sensitivity caused by H19 knockdown.Conclusion: H19 confers TMZ resistance through activating NF-κB signaling and may represent a novel therapeutic target for TMZ-resistant gliomas. Keywords: H19, oxidative stress, TMZ resistance, NF-κB pathway, glioma&nbsp" @default.
• W2892975930 created "2018-10-05" @default.
• W2892975930 creator A5021384155 @default.
• W2892975930 creator A5024126340 @default.
• W2892975930 creator A5035282379 @default.
• W2892975930 creator A5048246173 @default.
• W2892975930 creator A5087746649 @default.
• W2892975930 date "2018-10-01" @default.
• W2892975930 modified "2023-09-26" @default.
• W2892975930 title "H19 induced by oxidative stress confers temozolomide resistance in human glioma cells via activating NF-&kappa;B signaling" @default.
• W2892975930 cites W1791218006 @default.
• W2892975930 cites W1913006625 @default.
• W2892975930 cites W1945958863 @default.
• W2892975930 cites W1964123122 @default.
• W2892975930 cites W1974350437 @default.
• W2892975930 cites W1976096075 @default.
• W2892975930 cites W2036044314 @default.
• W2892975930 cites W2046297101 @default.
• W2892975930 cites W2080122625 @default.
• W2892975930 cites W2089990689 @default.
• W2892975930 cites W2134807618 @default.
• W2892975930 cites W2151458602 @default.
• W2892975930 cites W2162757298 @default.
• W2892975930 cites W2212574056 @default.
• W2892975930 cites W2422515295 @default.
• W2892975930 cites W2508147595 @default.
• W2892975930 cites W2511206720 @default.
• W2892975930 cites W2584114288 @default.
• W2892975930 cites W2605006100 @default.
• W2892975930 cites W2623629471 @default.
• W2892975930 cites W2694108262 @default.
• W2892975930 cites W2742973339 @default.
• W2892975930 cites W2749896527 @default.
• W2892975930 cites W2761330139 @default.
• W2892975930 cites W2765241643 @default.
• W2892975930 cites W2766372894 @default.
• W2892975930 cites W2780260597 @default.
• W2892975930 cites W2784151783 @default.
• W2892975930 cites W2886145107 @default.
• W2892975930 cites W2995726900 @default.
• W2892975930 doi "https://doi.org/10.2147/ott.s173244" @default.
• W2892975930 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6174297" @default.
• W2892975930 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30323617" @default.
• W2892975930 hasPublicationYear "2018" @default.
• W2892975930 type Work @default.
• W2892975930 sameAs 2892975930 @default.
• W2892975930 citedByCount "27" @default.
• W2892975930 countsByYear W28929759302019 @default.
• W2892975930 countsByYear W28929759302020 @default.
• W2892975930 countsByYear W28929759302021 @default.
• W2892975930 countsByYear W28929759302022 @default.
• W2892975930 countsByYear W28929759302023 @default.
• W2892975930 crossrefType "journal-article" @default.
• W2892975930 hasAuthorship W2892975930A5021384155 @default.
• W2892975930 hasAuthorship W2892975930A5024126340 @default.
• W2892975930 hasAuthorship W2892975930A5035282379 @default.
• W2892975930 hasAuthorship W2892975930A5048246173 @default.
• W2892975930 hasAuthorship W2892975930A5087746649 @default.
• W2892975930 hasBestOaLocation W28929759301 @default.
• W2892975930 hasConcept C111335760 @default.
• W2892975930 hasConcept C126322002 @default.
• W2892975930 hasConcept C153911025 @default.
• W2892975930 hasConcept C173396325 @default.
• W2892975930 hasConcept C185592680 @default.
• W2892975930 hasConcept C190283241 @default.
• W2892975930 hasConcept C2776151105 @default.
• W2892975930 hasConcept C2777389519 @default.
• W2892975930 hasConcept C2778227246 @default.
• W2892975930 hasConcept C502942594 @default.
• W2892975930 hasConcept C54009773 @default.
• W2892975930 hasConcept C54355233 @default.
• W2892975930 hasConcept C55493867 @default.
• W2892975930 hasConcept C62478195 @default.
• W2892975930 hasConcept C71924100 @default.
• W2892975930 hasConcept C81885089 @default.
• W2892975930 hasConcept C86803240 @default.
• W2892975930 hasConcept C95444343 @default.
• W2892975930 hasConceptScore W2892975930C111335760 @default.
• W2892975930 hasConceptScore W2892975930C126322002 @default.
• W2892975930 hasConceptScore W2892975930C153911025 @default.
• W2892975930 hasConceptScore W2892975930C173396325 @default.
• W2892975930 hasConceptScore W2892975930C185592680 @default.
• W2892975930 hasConceptScore W2892975930C190283241 @default.
• W2892975930 hasConceptScore W2892975930C2776151105 @default.
• W2892975930 hasConceptScore W2892975930C2777389519 @default.
• W2892975930 hasConceptScore W2892975930C2778227246 @default.
• W2892975930 hasConceptScore W2892975930C502942594 @default.
• W2892975930 hasConceptScore W2892975930C54009773 @default.
• W2892975930 hasConceptScore W2892975930C54355233 @default.
• W2892975930 hasConceptScore W2892975930C55493867 @default.
• W2892975930 hasConceptScore W2892975930C62478195 @default.
• W2892975930 hasConceptScore W2892975930C71924100 @default.
• W2892975930 hasConceptScore W2892975930C81885089 @default.
• W2892975930 hasConceptScore W2892975930C86803240 @default.
• W2892975930 hasConceptScore W2892975930C95444343 @default.
• W2892975930 hasLocation W28929759301 @default.
• W2892975930 hasLocation W28929759302 @default.
• W2892975930 hasLocation W28929759303 @default.

• next