PT  - JOURNAL ARTICLE
AU  - DAN-PING XIE
AU  - YI-XI GONG
AU  - YING-HUA JIN
AU  - CHEN-XI REN
AU  - YUE LIU
AU  - YING-HAO HAN
AU  - MEI-HUA JIN
AU  - DAN ZHU
AU  - QIU-ZHEN PAN
AU  - LI-YUN YU
AU  - DONG-SEOK LEE
AU  - JAIHYUNG LEE
AU  - JIHWAN KIM
AU  - YANG HO PARK
AU  - JIN WON HYUN
AU  - TAEHO KWON
AU  - YU-DONG CUI
AU  - HU-NAN SUN
TI  - Anti-tumor Properties of <em>Picrasma quassioides</em> Extracts in H-Ras<sup>G12V</sup> Liver Cancer Are Mediated Through ROS-dependent Mitochondrial Dysfunction
AID  - 10.21873/anticanres.14371
DP  - 2020 Jul 01
TA  - Anticancer Research
PG  - 3819--3830
VI  - 40
IP  - 7
4099  - http://ar.iiarjournals.org/content/40/7/3819.short
4100  - http://ar.iiarjournals.org/content/40/7/3819.full
SO  - Anticancer Res2020 Jul 01; 40
AB  - Background: Picrasma quassioides (PQ) is a traditional Asian herbal medicine with anti-tumor properties that can inhibit the viability of HepG2 liver cancer cells. H-Ras is often mutated in liver cancer, however, the effect of PQ treatment on H-Ras mutated liver cancer is unclear. This study aimed to investigate the role of PQ on ROS accumulation and mitochondrial dysfunction in H-ras mutated HepG2 (HepG2G12V) cells. Materials and Methods: PQ ethanol extract-induced HepG2G12V apoptosis was analyzed by the MTT assay, fluorescence microscopy, flow cytometry and western blotting. Results: PQ treatment affected cell migration and colony formation in HepG2G12V cells. Cleaved-caspase-3, cleaved-caspase-9 and BCL2 associated agonist of cell death (BAD) expression levels were increased, while the levels of B-cell lymphoma-extra large (Bcl-xL) were decreased with PQ treatment. PQ treatment led to a reduction of H-Ras expression levels in liver cancer cells, thus reducing their abnormal proliferation. Furthermore, it led to increased expression levels of Peroxiredoxin VI, which regulates the redox signal in cells. Conclusion: Taken together these results provide a new functional significance for the role of PQ in treating HepG2G12V liver cancer.