Conference PaperPDF Available

Frankincense as a Potentially Novel Therapeutic Agent in Ovarian Cancer

  • February 2015
DOI:10.13140/2.1.1016.2241
  • Conference: 27th Lorne Cancer Conference 2015
  • At: Mantra Lorne, Lorne, Victoria, Australia
Authors:
Kamla K Al Salmani at Ministry of Health, Sultanate of Oman
Kamla K Al Salmani
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Abstract

Frankincense as a Potentially Novel Therapeutic Agent in Ovarian Cancer Kamla Al Salmani1, Esther Moss1, Don Jones2, Raj Patel2, Ikram Burney3, Mark D. Evans1 1Department of Cancer Studies,& 2Department of Biochemistry, University of Leicester; 3Department of Oncology, Sultan Qaboos University, Oman. This study examines the biologically active component of Frankincense, 3-O-acetyl-11-keto-β-boswellic acid (AKBA), in ovarian cancer cells, to evaluate its potential cytotoxicity towards 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, at stage IIIa-IIIc and stage IV. Majority 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 properties and anti-cancer potential alone or in combination with other chemotherapies. The active ingredients of Boswellia sp., boswellic acids, have many effects on various cancer cells including induction of apoptosis. 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 after16 hours or more. Significant cell death was observed at 25µM 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. Cell cycle analysis showed evidence of cell cycle arrest at G1 following AKBA treatment, dependent on concentration and time of exposure. AKBA is cytotoxic to ovarian cancer cells, at pharmacologically achievable concentrations. AKBA also induces DNA damage and G1arrest. AKBA may form the basis of a novel anticancer treatment for ovarian cancer perhaps alongside conventional chemotherapy.
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