Format

Send to

Choose Destination
Anticancer Drugs. 2018 Sep;29(8):756-766. doi: 10.1097/CAD.0000000000000646.

Ginsenoside Rg1 impairs homologous recombination repair by targeting CtBP-interacting protein and sensitizes hepatoblastoma cells to DNA damage.

Author information

1
Department of Laboratory Medicine, Shanghai Children’s Medical Center, School of medicine, Shanghai Jiaotong University.
2
Department of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University.
3
Department of Medical Laboratory, College of Allied Health Professions, Shanghai University of Medicine and Health Sciences.
4
Department of Surgery, Shanghai Children’s Medical Center, School of medicine, Shanghai Jiaotong University.
5
Department of Gynecology, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.

Abstract

The ginsenoside Rg1, the primary pharmacologically active ingredient of the traditional Chinese herb ginseng, is widely used in the clinical treatment of diseases of the immune and nervous systems. Recent studies have shown that it also has an antitumor effect. In this study, we explored the effects of Rg1 on hepatoblastoma (HB) and its underlying mechanisms. We demonstrated that Rg1 significantly inhibited HB cell growth both in vivo and in vitro. Mechanistic studies revealed that Rg1 impaired homologous recombination and triggered double-strand breaks in HB cells by directly targeting CtBP-interacting protein (CtIP), a key double-strand break repair factor, which is highly expressed in HB tissues. Moreover, we also demonstrated that Rg1 sensitized HB cells to DNA-damaging agents both in vitro and in vivo. In conclusion, our data not only demonstrate the potential clinical application of Rg1 as a novel chemotherapeutic candidate but also offer a mechanism-based therapeutic option by which DNA-damaging agents can be used in combination with Rg1 to target HB.

PMID:
29952772
DOI:
10.1097/CAD.0000000000000646
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center