FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2332637124> ?p ?o ?g. }

• W2332637124 endingPage "342" @default.
• W2332637124 startingPage "331" @default.
• W2332637124 abstract "3β-O-{α-L-Pyran rhamnose-(1→3)-[β-D-xylopyranose-(1→2)]-β-D-glucopyranose-(1→4)-[β-D-lucopyranose-(1→2)]-α-L-pyran arabinose}-cyclamiretin A (AG4) is a saponin component obtained from the Giantleaf Ardisia Rhizome (Rhizoma Ardisiae Gigantifoliae). The present study aimed to investigate the antitumor potential of AG4 and its possible mechanisms in human nasopharyngeal carcinoma cells (CNE). We exposed tumor cells to AG4 to investigate which cell line was the most sensitive to AG4. Cell viability was assessed using the MTT reduction assay, and the effects of AG4 on apoptosis, reactive oxygen species (ROS) content, mitochondrial membrane potential (MMP), and cell cycle were detected using a flow cytometer; the glutathione, superoxide dismutase and malondialdehyde activities were measured using colorimetric methods. The relative expressions of Bax, Bad, Bid, Bcl-2, and Fas mRNA were calculated using the (Equation is included in full-text article.)comparative method by real-time PCR studies and protein was detected by western blotting. AG4 markedly inhibited the growth of CNE cells by decreasing cell proliferation, inducing apoptosis, and blocking the cell cycle in the S phase. The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK). Moreover, the MMP was decreased in AG4-treated cells, and AG4-induced cell apoptosis was accompanied by a rapid and lasting increase in ROS, which was abolished by N-acetyl-L-cysteine (NAC); glutathione, superoxide dismutase, and malondialdehyde were regulated by AG4. AG4 inhibited Bcl-2 mRNA and protein expression and stimulated Bax, Bad, Bid, Fas mRNA, and protein expression in CNE cultures, suggesting an effect at the transcriptional and protein level. In addition, both the FasL inhibitor (AF-016) and the Bcl-2 family inhibitor (GX15-070) could prevent the cell apoptosis induced by AG4. The findings suggested that AG4-induced apoptosis in CNE cells involved a death receptor pathway and a Bcl-2 family-mediated mitochondrial signaling pathway by decreasing the MMPs in an ROS-dependent manner and regulating genes and proteins relative to apoptosis; also, regulation of cell cycles may also play a role in the antitumor mechanism of AG4." @default.
• W2332637124 created "2016-06-24" @default.
• W2332637124 creator A5014075355 @default.
• W2332637124 creator A5039839914 @default.
• W2332637124 creator A5044931995 @default.
• W2332637124 creator A5045940268 @default.
• W2332637124 creator A5068137442 @default.
• W2332637124 creator A5072270785 @default.
• W2332637124 creator A5077153113 @default.
• W2332637124 creator A5084555879 @default.
• W2332637124 date "2015-03-01" @default.
• W2332637124 modified "2023-10-16" @default.
• W2332637124 title "AG4, a compound isolated from Radix Ardisiae Gigantifoliae, induces apoptosis in human nasopharyngeal cancer CNE cells through intrinsic and extrinsic apoptosis pathways" @default.
• W2332637124 cites W116732461 @default.
• W2332637124 cites W1495037894 @default.
• W2332637124 cites W1571529930 @default.
• W2332637124 cites W1658347783 @default.
• W2332637124 cites W1967049800 @default.
• W2332637124 cites W1970408491 @default.
• W2332637124 cites W1980078856 @default.
• W2332637124 cites W1980100638 @default.
• W2332637124 cites W1987676467 @default.
• W2332637124 cites W1988655372 @default.
• W2332637124 cites W2000877238 @default.
• W2332637124 cites W2005782076 @default.
• W2332637124 cites W2006941663 @default.
• W2332637124 cites W2007007231 @default.
• W2332637124 cites W2015424171 @default.
• W2332637124 cites W2018077387 @default.
• W2332637124 cites W2036411709 @default.
• W2332637124 cites W2047937356 @default.
• W2332637124 cites W2060435320 @default.
• W2332637124 cites W2062499210 @default.
• W2332637124 cites W2071675514 @default.
• W2332637124 cites W2078511129 @default.
• W2332637124 cites W2081605103 @default.
• W2332637124 cites W2102772371 @default.
• W2332637124 cites W2128179846 @default.
• W2332637124 cites W2320101893 @default.
• W2332637124 cites W2326539506 @default.
• W2332637124 cites W3004118171 @default.
• W2332637124 doi "https://doi.org/10.1097/cad.0000000000000193" @default.
• W2332637124 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25521557" @default.
• W2332637124 hasPublicationYear "2015" @default.
• W2332637124 type Work @default.
• W2332637124 sameAs 2332637124 @default.
• W2332637124 citedByCount "6" @default.
• W2332637124 countsByYear W23326371242015 @default.
• W2332637124 countsByYear W23326371242016 @default.
• W2332637124 countsByYear W23326371242017 @default.
• W2332637124 countsByYear W23326371242022 @default.
• W2332637124 countsByYear W23326371242023 @default.
• W2332637124 crossrefType "journal-article" @default.
• W2332637124 hasAuthorship W2332637124A5014075355 @default.
• W2332637124 hasAuthorship W2332637124A5039839914 @default.
• W2332637124 hasAuthorship W2332637124A5044931995 @default.
• W2332637124 hasAuthorship W2332637124A5045940268 @default.
• W2332637124 hasAuthorship W2332637124A5068137442 @default.
• W2332637124 hasAuthorship W2332637124A5072270785 @default.
• W2332637124 hasAuthorship W2332637124A5077153113 @default.
• W2332637124 hasAuthorship W2332637124A5084555879 @default.
• W2332637124 hasConcept C126322002 @default.
• W2332637124 hasConcept C153911025 @default.
• W2332637124 hasConcept C185592680 @default.
• W2332637124 hasConcept C190283241 @default.
• W2332637124 hasConcept C2775838275 @default.
• W2332637124 hasConcept C2776151105 @default.
• W2332637124 hasConcept C2778401633 @default.
• W2332637124 hasConcept C2778997737 @default.
• W2332637124 hasConcept C2780783641 @default.
• W2332637124 hasConcept C29537977 @default.
• W2332637124 hasConcept C48349386 @default.
• W2332637124 hasConcept C509974204 @default.
• W2332637124 hasConcept C53227056 @default.
• W2332637124 hasConcept C55493867 @default.
• W2332637124 hasConcept C71924100 @default.
• W2332637124 hasConcept C86803240 @default.
• W2332637124 hasConcept C95444343 @default.
• W2332637124 hasConceptScore W2332637124C126322002 @default.
• W2332637124 hasConceptScore W2332637124C153911025 @default.
• W2332637124 hasConceptScore W2332637124C185592680 @default.
• W2332637124 hasConceptScore W2332637124C190283241 @default.
• W2332637124 hasConceptScore W2332637124C2775838275 @default.
• W2332637124 hasConceptScore W2332637124C2776151105 @default.
• W2332637124 hasConceptScore W2332637124C2778401633 @default.
• W2332637124 hasConceptScore W2332637124C2778997737 @default.
• W2332637124 hasConceptScore W2332637124C2780783641 @default.
• W2332637124 hasConceptScore W2332637124C29537977 @default.
• W2332637124 hasConceptScore W2332637124C48349386 @default.
• W2332637124 hasConceptScore W2332637124C509974204 @default.
• W2332637124 hasConceptScore W2332637124C53227056 @default.
• W2332637124 hasConceptScore W2332637124C55493867 @default.
• W2332637124 hasConceptScore W2332637124C71924100 @default.
• W2332637124 hasConceptScore W2332637124C86803240 @default.
• W2332637124 hasConceptScore W2332637124C95444343 @default.
• W2332637124 hasIssue "3" @default.
• W2332637124 hasLocation W23326371241 @default.
• W2332637124 hasLocation W23326371242 @default.

• next