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Details

Autor(en) / Beteiligte
Titel
Maintenance of the Expression of c-FLIPL by Hsp70 to Resist Licochalcone A-Induced Anti-Colorectal Cancer Effect through ERK-Mediated Autophagy Induction
Ist Teil von
  • Frontiers in bioscience (Landmark. Print), 2023-12, Vol.28 (12), p.325-325
Ort / Verlag
IMR Press
Erscheinungsjahr
2023
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • BACKGROUNDThe mortality rate of colorectal cancer (CRC) ranks second worldwide. Previous research had indicated that licochalcone A (LA) was a flavonoid in licorice with diverse anticancer effects. We explored the underlying mechanisms of LA-triggered anticancer activity in CRC.METHODSThiazolyl Blue (MTT) experiment and EdU staining were utilized to evaluate cell proliferation. Meanwhile, cells were stained by Annexin V/PI to investigate apoptosis through flow cytometry assay. Moreover, expressions of proteins were detected by immunoblotting, and the level of related mRNA was investigated using real-time quantitative PCR.RESULTSLA selectively suppressed the proliferation and triggered apoptosis of CRC cells. Strikingly, LA induced cytoprotective autophagic activities since the suppression of autophagy significantly strengthened LA-induced cytotoxicity and FLICE inhibitory protein (c-FLIPL) degradation, meanwhile reversing LA-mediated heat shock protein 70 (Hsp70) upregulation. Moreover, autophagy-mediated Hsp70 upregulation resisted LA-induced anticancer effects since the suppression of Hsp70 strengthened LA-triggered cytotoxicity and c-FLIPL degradation. Furthermore, LA greatly activated extracellular signal-regulated protein kinases (ERK) and p38. However, blocking of ERK, but not p38, significantly boosted LA-triggered cell death and c-FLIPL downregulation. Suppression of ERK also reversed LA-mediated autophagic induction.CONCLUSIONSLA increased Hsp70 expression depending on ERK-mediated autophagy, which protected CRC cells from LA-induced anticancer activities.
Sprache
Englisch
Identifikatoren
ISSN: 2768-6701
eISSN: 2768-6698
DOI: 10.31083/j.fbl2812325
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_606914616b444ed18dcaee82cd25ece4

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