Isocorydine suppresses doxorubicin-induced epithelial-mesenchymal transition via inhibition of ERK signaling pathways in hepatocellular carcinoma.
Am J Cancer Res
; 8(1): 154-164, 2018.
Article
en En
| MEDLINE
| ID: mdl-29416928
ABSTRACT
Doxorubicin (DOX) is a conventional and effective chemotherapeutic used in the treatment of hepatocellular carcinoma (HCC). However, doxorubicin administration may induce EMT, which results in the development of chemoresistance in HCC. Recent studies report that Isocorydine (ICD) selectively inhibits human cancer stem cells (CSCs), which have an important role in the development of chemoresistance. In this study, we observed that ICD co-administration enhanced DOX cytotoxicity in HCC cells, enabling the inhibition of DOX-induced epithelial-mesenchymal transition (EMT). Microarray data analysis revealed substantially decreased ERK signaling after ICD treatment. Additionally, we observed decreased IC50 for DOX upon ERK knockdown. Finally, we confirmed the enhanced efficacy of treatment with a combination of DOX and ICD in xenograft models. Collectively, the present study unveils the benefit of using DOX in combination with ICD for chemotherapy against HCC, revealing a novel potential anti-cancer strategy.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
Am J Cancer Res
Año:
2018
Tipo del documento:
Article
País de afiliación:
China