Matches in SemOpenAlex for { <https://semopenalex.org/work/W4385985029> ?p ?o ?g. }
Showing items 1 to 85 of
85
with 100 items per page.
- W4385985029 endingPage "170" @default.
- W4385985029 startingPage "170" @default.
- W4385985029 abstract "Background: The role of Pin2 telomeric repeat factor 1-interacting telomerase inhibitor 1 (PinX1) in tumorigenesis and development has been extensively studied. As we previously demonstrated, PinX1 plays an important role in modulating epithelial-mesenchymal transition (EMT), stemness, cell proliferation, and apoptosis in nasopharyngeal carcinoma (NPC). However, the relationship between PinX1, autophagy, and cell function in NPC remains unclear. This study aimed to investigate the mechanisms by which PinX1 regulates autophagy in NPC, and to explore its biological role and clinical significance in disease progression. Methods: The proliferative capacity of NPC cells was assessed by MTT and xenograft tumorigenicity assays. Autophagic flux was monitored using a tandem monomeric DAPI–FITC–LC3 reporter assay. The rates of apoptosis and the cell cycle in NPC cells were analyzed using flow cytometry. The activation of autophagy and the signaling status of the AKT/mTOR and NF-κB/p65 pathways were evaluated by Western blot analysis. Results: In addition to promoting autophagy and apoptosis, PinX1 overexpression suppressed proliferation, migration, invasion, and decelerated cell-cycle progression in NPC cells. These effects were reversed by inhibiting autophagy with 3-methyladenine. Mechanistic investigations clarified that PinX1 overexpression significantly reduced the expression of p-AKT, p-mTOR, p65, and p-p65. Chloroquine treatment in PinX1-overexpressing cells did not significantly alter p-AKT and p-mTOR levels, whereas 3-MA treatment in PinX1-overexpressing cells resulted in increased p65 and p-p65 expression, relative to untreated PinX1-overexpressing cells. Conclusions: It appears that PinX1 promotes autophagy by inhibiting the AKT/mTOR signaling pathway, which then inhibits NF-κB/p65 pathways, and consequently inhibiting cell proliferation and causing cell apoptosis in NPC cells." @default.
- W4385985029 created "2023-08-19" @default.
- W4385985029 creator A5042779459 @default.
- W4385985029 creator A5058551421 @default.
- W4385985029 creator A5059146155 @default.
- W4385985029 creator A5059184457 @default.
- W4385985029 creator A5060339883 @default.
- W4385985029 creator A5069732404 @default.
- W4385985029 creator A5071999920 @default.
- W4385985029 creator A5073420488 @default.
- W4385985029 creator A5080841020 @default.
- W4385985029 date "2023-08-17" @default.
- W4385985029 modified "2023-09-25" @default.
- W4385985029 title "PinX1-Promoted Autophagy Inhibits Cell Proliferation and Induces Cell Apoptosis by Inhibiting the NF-κB/p65 Signaling Pathway in Nasopharyngeal Carcinoma" @default.
- W4385985029 doi "https://doi.org/10.31083/j.fbl2808170" @default.
- W4385985029 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37664923" @default.
- W4385985029 hasPublicationYear "2023" @default.
- W4385985029 type Work @default.
- W4385985029 citedByCount "0" @default.
- W4385985029 crossrefType "journal-article" @default.
- W4385985029 hasAuthorship W4385985029A5042779459 @default.
- W4385985029 hasAuthorship W4385985029A5058551421 @default.
- W4385985029 hasAuthorship W4385985029A5059146155 @default.
- W4385985029 hasAuthorship W4385985029A5059184457 @default.
- W4385985029 hasAuthorship W4385985029A5060339883 @default.
- W4385985029 hasAuthorship W4385985029A5069732404 @default.
- W4385985029 hasAuthorship W4385985029A5071999920 @default.
- W4385985029 hasAuthorship W4385985029A5073420488 @default.
- W4385985029 hasAuthorship W4385985029A5080841020 @default.
- W4385985029 hasBestOaLocation W43859850291 @default.
- W4385985029 hasConcept C126322002 @default.
- W4385985029 hasConcept C153911025 @default.
- W4385985029 hasConcept C185592680 @default.
- W4385985029 hasConcept C190283241 @default.
- W4385985029 hasConcept C203522944 @default.
- W4385985029 hasConcept C2778997737 @default.
- W4385985029 hasConcept C29537977 @default.
- W4385985029 hasConcept C502942594 @default.
- W4385985029 hasConcept C509974204 @default.
- W4385985029 hasConcept C55493867 @default.
- W4385985029 hasConcept C62112901 @default.
- W4385985029 hasConcept C62478195 @default.
- W4385985029 hasConcept C71924100 @default.
- W4385985029 hasConcept C75217442 @default.
- W4385985029 hasConcept C86554907 @default.
- W4385985029 hasConcept C86803240 @default.
- W4385985029 hasConcept C95444343 @default.
- W4385985029 hasConceptScore W4385985029C126322002 @default.
- W4385985029 hasConceptScore W4385985029C153911025 @default.
- W4385985029 hasConceptScore W4385985029C185592680 @default.
- W4385985029 hasConceptScore W4385985029C190283241 @default.
- W4385985029 hasConceptScore W4385985029C203522944 @default.
- W4385985029 hasConceptScore W4385985029C2778997737 @default.
- W4385985029 hasConceptScore W4385985029C29537977 @default.
- W4385985029 hasConceptScore W4385985029C502942594 @default.
- W4385985029 hasConceptScore W4385985029C509974204 @default.
- W4385985029 hasConceptScore W4385985029C55493867 @default.
- W4385985029 hasConceptScore W4385985029C62112901 @default.
- W4385985029 hasConceptScore W4385985029C62478195 @default.
- W4385985029 hasConceptScore W4385985029C71924100 @default.
- W4385985029 hasConceptScore W4385985029C75217442 @default.
- W4385985029 hasConceptScore W4385985029C86554907 @default.
- W4385985029 hasConceptScore W4385985029C86803240 @default.
- W4385985029 hasConceptScore W4385985029C95444343 @default.
- W4385985029 hasIssue "8" @default.
- W4385985029 hasLocation W43859850291 @default.
- W4385985029 hasLocation W43859850292 @default.
- W4385985029 hasOpenAccess W4385985029 @default.
- W4385985029 hasPrimaryLocation W43859850291 @default.
- W4385985029 hasRelatedWork W1585268103 @default.
- W4385985029 hasRelatedWork W2031322368 @default.
- W4385985029 hasRelatedWork W2127153258 @default.
- W4385985029 hasRelatedWork W2147371753 @default.
- W4385985029 hasRelatedWork W2438578109 @default.
- W4385985029 hasRelatedWork W2939274558 @default.
- W4385985029 hasRelatedWork W3002644491 @default.
- W4385985029 hasRelatedWork W3089957099 @default.
- W4385985029 hasRelatedWork W3140193828 @default.
- W4385985029 hasRelatedWork W3155888605 @default.
- W4385985029 hasVolume "28" @default.
- W4385985029 isParatext "false" @default.
- W4385985029 isRetracted "false" @default.
- W4385985029 workType "article" @default.