Inactivation of EGFR/ERK/NF-κB signalling associates with radiosensitizing effect of 18ß-glycyrrhetinic acid on progression of hepatocellular carcinoma.
J Cell Mol Med
; 27(11): 1539-1549, 2023 06.
Article
en En
| MEDLINE
| ID: mdl-37177859
ABSTRACT
Hepatocellular carcinoma (HCC) is recognized as the fifth most common cancer and the third most common cause of death in Asian population. Studies reported that HCC is relatively insensitive to radiotherapy (RT); thus, considering how to sensitize HCC to RT is worth to be elucidated. Epidermal growth factor receptor (EGFR)-mediated signalling transduction plays the important role in regulating treatment efficacy of HCC. An active compound, 18beta-glycyrrhetinic acid (18ß-GA), has been reported to own anti-tumour effect. However, whether 18ß-GA possess RT sensitization ability in HCC remains unclear. Here, we used RNA data from TCGA-LIHC (Liver hepatocellular carcinoma) to identify the role between EGFR/ERK/nuclear factor kappa B (NF-κB) signalling and RT by radiosensitivity index (RSI) analysis. We suggested that patients with activated NF-κB signalling may show resistance to RT treatment, whereas combining 18ß-GA may reinforce RT efficacy in a Hep3B-bearing animal model. 18ß-GA combined with RT showed superior tumour inhibition capacity as compared to monotherapy and even reached similar efficacy as erlotinib combined with RT. Treatment promotion of RT by 18ß-GA in HCC is not only through diminishing RT-induced EGFR/ERK/NF-κB signalling but also promoting RT-induced apoptosis pathways. 18ß-GA may act as radiosensitizer through inactivating EGFR-mediated HCC progression and inducing caspase-dependent apoptosis signalling.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Fármacos Sensibilizantes a Radiaciones
/
Carcinoma Hepatocelular
/
Neoplasias Hepáticas
Tipo de estudio:
Prognostic_studies
/
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
J Cell Mol Med
Asunto de la revista:
BIOLOGIA MOLECULAR
Año:
2023
Tipo del documento:
Article
País de afiliación:
Taiwán