Anti-tumor activity of HIS-4,a biflavonoid from Resina draconis,on human hepatoma HepG2 and SK-HEP-1 cells / 中国中药杂志
China Journal of Chinese Materia Medica
;
(24): 1442-1449, 2019.
Artículo
en Chino
| WPRIM
| ID: wpr-774537
ABSTRACT
The research of anti-hepatocellular carcinoma(HCC) drug has attracted more and more attention. Natural products are the important source of active compounds for cancer treatment. A biflavonoid HIS-4 was isolated from Resina draconis in our previous study. MTT assay, hoechst staining, and flow cytometry analysis were used to investigate the effects of HIS-4 on the proliferation and apoptosis of human hepatoma HepG2 and SK-HEP-1 cells. Moreover, the effects of HIS-4 on the migration and invasion ability of HepG2 and SK-HEP-1 cells were evaluated by wound healing assay and Transwell assay. In addition, MTT assay, flow cytometry analyses, Hoechst staining, wound healing assay, Transwell assay, and tube formation assay were used to explore the anti-angiogenic activity of HIS-4 in human umbilical vein endothelial cells(HUVECs). Mechanistically, the HIS-4 regulatory of signal pathways in H9 epG2 and SK-HEP-1 cells were analyzed by Western blot. This results showed that HIS-4 suppressed the proliferation of human hepatoma HepG2 and SK-HEP-1 cells. Moreover HIS-4 induced their apoptosis of HepG2 and SK-HEP-1 cells. HIS-4 inhibited the migration and invasion of HepG2 and SK-HEP-1 cells. Additionally, HIS-4 exhibited angiogenesis effects. Mechanistically, up-regulation of MAPK signaling pathway and down-regulation of mTOR signaling pathway may be responsible for anti-hepatoma activity of HIS-4. Therefore, HIS-4 may be a promising candidate drug for HCC treatment.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Farmacología
/
Movimiento Celular
/
Química
/
Apoptosis
/
Carcinoma Hepatocelular
/
Dracaena
/
Biflavonoides
/
Proliferación Celular
/
Quimioterapia
Límite:
Humanos
Idioma:
Chino
Revista:
China Journal of Chinese Materia Medica
Año:
2019
Tipo del documento:
Artículo
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