A82: Frankincense as a Potentially Novel Therapeutic Agent in Ovarian Cancer

Kamla Al-Salmani1,Esther Moss1,Don Jones1,Raj Patel2,Ikram Burney4,Ahmed Al-Harassi5,Mark D. Evans1,3

1Department of Cancer Studies, University of Leicester, Leicester, UK,2Department of Biochemistry, University of Leicester, Leicester, UK,3School of Allied Health Sciences, De Montfort University, Leicester, UK,4Department of Oncology, Sultan Qaboos University, Muscat, Oman,5University of Nizwa, Nizwa, Oman

Presenting date: Monday 2 November
Presenting time: 13.10-14.00

Background

 This study examines the biologically active component of Frankincense, 3-O-acetyl-11-keto-?-boswellic acid (AKBA), in ovarian cancer cells, to evaluate its potential cytotoxicity towards with high grade serous ovarian cancer and its ability to subvert resistance to cisplatin.

Ovarian cancer causes significant mortality, the five year survival rate is very low compared to other cancers, and most of the cases are diagnosed late. Most of these cases relapse and develop resistance to first line chemotherapy; therefore new strategies are urgently needed to overcome resistance. Extracts from Boswellia sp., used for centuries as herbal medicine in Asia, have known anti-inflammatory[1] properties and anti-cancer potential[2]. The active ingredients of Boswellia sp., boswellic acids, have many effects on various cancer cells including induction of apoptosis[3].

Method

Comet assay was used to detect the deoxyribonucleic acid (DNA) damage, flow cytometry to examine the cell cycle arrest, Annexin IV/PI for apoptosis, western blotting, Microarray and QPCR to confirm the specific apoptotic proteins expressions

Results

  

50µM AKBA induced significant (P<0.001) DNA damage (strand breaks and alkali-labile sites) immediately in all ovarian cancer cell lines compared to controls treated only with DMSO, whereas 15 µM and 25 µM AKBA induced significant DNA damage after 16 hours or more.  Significant cell death was observed at 15µM AKBA or higher, dependent on the exposure time, in all cell lines [OVCAR 4, UWB 1.289, A2780 and A2780-cis (cisplatin-resistant)]. OVCAR4 and A2780cis cell lines were significantly more sensitive to the cytotoxic effects of AKBA.

Conclusion

 AKBA is cytotoxic to ovarian cancer cells, at pharmacologically achievable concentrations.  AKBA exposure also induces multiple gene expression in different biological pathways in ovarian cancer cells.  AKBA may form the basis of a novel anticancer treatment for ovarian cancer perhaps alongside conventional chemotherapy.