Zeitschrift
- Titel:
- Open medicine
- Erschienen:
-
Berlin: de Gruyter
- Fußnote:
- Open Access
- Namensnennung 4.0 International
- Umfang:
- Online-Ressource
- ISSN:
- 2391-5463
- ZDB-ID:
-
2829380-0
- VÖBB-Katalog:
- 35318930
- Schlagworte:
- Zeitschrift
- Dewey-Dezimalklassifikation:
- 610 Medizin
- Copyright:
- Rechte vorbehalten
- Zugriffsberechtigung:
- Freier Zugang
- Titel:
- Open medicine
- Erschienen:
-
Berlin: de Gruyter
- Fußnote:
- Open Access
- Namensnennung 4.0 International
- Umfang:
- Online-Ressource
- ISSN:
- 2391-5463
- ZDB-ID:
-
2829380-0
- VÖBB-Katalog:
- 35318930
- Schlagworte:
- Zeitschrift
- Dewey-Dezimalklassifikation:
- 610 Medizin
- Copyright:
- Rechte vorbehalten
- Zugriffsberechtigung:
- Freier Zugang
Aufsatz
- Titel:
- The H2Valdien derivatives regulate the epithelial–mesenchymal transition of hepatoma carcinoma cells through the Hedgehog signaling pathway
- Erschienen:
-
Berlin: de Gruyter, 2024
- Sprache:
- Englisch
- Zusammenfassung:
- Abstract: This research delves into the influence of H2Valdien derivatives on the proliferation, migration, and apoptosis induction in hepatoma carcinoma cells (HepG2, Huh-7, and SMMC-7721), with a specific emphasis on inhibiting epithelial–mesenchymal transition (EMT) through modulation of the Hedgehog (Hh) signaling pathway. Utilizing the cell counting kit-8 method, flow cytometry, TUNEL assay, wound healing, and transwell assays, we observed a dose-dependent growth arrest and apoptosis induction in HepG2, Huh-7, and SMMC-7721 cells. Notably, H2Valdien derivatives exhibited a capacity to reduce migration and invasion, impacting the expression of EMT-associated proteins such as N-cadherin, vimentin, and E-cadherin. Mechanistically, these derivatives demonstrated the inhibition of the Hh signaling pathway by inactivating Sonic Hh (Shh) and smoothened proteins. This study underscores the robust antiproliferative and apoptosis-inducing effects of H2Valdien derivatives on hepatoma carcinoma cells and elucidates their regulatory role in EMT through modulation of the Hh signaling pathway, providing valuable insights for potential therapeutic interventions.
- Umfang:
- Online-Ressource
- Fußnote:
- Open Access
- Archivierung/Langzeitarchivierung gewährleistet
- Schlagworte:
- H 2 Valdien derivatives ; Hh signaling pathway ; EMT ; hepatoma carcinoma
- ZLB-Systematik:
- Medizin
- Sammlung:
- Medizin
- Copyright:
- CC BY
- Zugriffsberechtigung:
- Freier Zugang
- Titel:
- The H2Valdien derivatives regulate the epithelial–mesenchymal transition of hepatoma carcinoma cells through the Hedgehog signaling pathway
- Erschienen:
-
Berlin: de Gruyter, 2024
- Sprache:
- Englisch
- Zusammenfassung:
- Abstract: This research delves into the influence of H2Valdien derivatives on the proliferation, migration, and apoptosis induction in hepatoma carcinoma cells (HepG2, Huh-7, and SMMC-7721), with a specific emphasis on inhibiting epithelial–mesenchymal transition (EMT) through modulation of the Hedgehog (Hh) signaling pathway. Utilizing the cell counting kit-8 method, flow cytometry, TUNEL assay, wound healing, and transwell assays, we observed a dose-dependent growth arrest and apoptosis induction in HepG2, Huh-7, and SMMC-7721 cells. Notably, H2Valdien derivatives exhibited a capacity to reduce migration and invasion, impacting the expression of EMT-associated proteins such as N-cadherin, vimentin, and E-cadherin. Mechanistically, these derivatives demonstrated the inhibition of the Hh signaling pathway by inactivating Sonic Hh (Shh) and smoothened proteins. This study underscores the robust antiproliferative and apoptosis-inducing effects of H2Valdien derivatives on hepatoma carcinoma cells and elucidates their regulatory role in EMT through modulation of the Hh signaling pathway, providing valuable insights for potential therapeutic interventions.
- Umfang:
- Online-Ressource
- Fußnote:
- Open Access
- Archivierung/Langzeitarchivierung gewährleistet
- Schlagworte:
- H 2 Valdien derivatives ; Hh signaling pathway ; EMT ; hepatoma carcinoma
- ZLB-Systematik:
- Medizin
- Sammlung:
- Medizin
- Copyright:
- CC BY
- Zugriffsberechtigung:
- Freier Zugang
