Leukemia Research

Volume 23, Issue 1, January 1999, Pages 43–50

"Boswellic acid acetate (BC-4), a compound isolated from the herb Boswellia carterii Birdw., can induce differentiation and apoptosis of leukemia cells...The dual apoptotic and differentiation effects of BC-4 suggest that it may be a powerful agent in the treatment of leukemia."

Boswellic acid acetate induces differentiation and apoptosis in leukemia cell lines

• Yongkui Jing^a, d, , 
• Shigeo Nakajo^c, 
• Lijuan Xia^a, 
• Kusuyasu Nakaya^c, 
• Qicheng Fang^b, 
• Samuel Waxman^d, 
• Rui Han^a

• ^a Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China
• ^b Department of Phytochemistry, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China
• ^c Department of Biological Chemistry, Showa University, Tokyo, Japan
• ^d Mount Sinai Medical Center, Box 1178, 1 Gustave L. Levy Place, New York, NY 10029, USA

Received 10 February 1998, Revised 1 May 1998, Accepted 5 May 1998, Available online 28 October 1998

 Abstract

Boswellic acid acetate (BC-4), a compound isolated from the herb Boswellia carterii Birdw., can induce differentiation and apoptosis of leukemia cells. Based on cell morphology and NBT reduction, BC-4 induced monocytic differentiation of myeloid leukemia HL-60, U937 and ML-1 cells at a dose under 12.5 μg/ml (24.2 μM). BC-4 was a potent inducer, with 90% of the cells showing morphologic changes and 80–90% of the cells showing NBT reduction. Specific and non-specific esterase were also increased by BC-4. Based on benzidine staining assay, BC-4 failed to induce erythroid leukemia DS-19 and K562 cells differentiation. In contrast to its selective differentiation effect, BC-4 strongly inhibited growth of all cell lines tested. The growth inhibition effect was dose- and time-dependent. In HL-60 cells, 20 μg/ml (38.8 μM) of BC-4 decreased viable cell number by 60% at 24 h, whereas at 3 days there was virtually no viable cells. Morphologic and DNA fragmentation analysis proved that BC-4 induced cell apoptosis. The dual apoptotic and differentiation effects of BC-4 suggest that it may be a powerful agent in the treatment of leukemia.

Keywords

• Boswellic acid acetate; 
• Leukemia; 
• Differentiation; 
• Apoptosis

Abbreviations

• 5-LO, 5-lipoxygenase; 
• TPA, 12-O-tetra-decanoylphorbol-13-acetate; 
• NBT nitroblue tetrazolium; 
• NSE, α-naphthyl acetate esterase; 
• SE, AS-D chloroacetate esterase

Corresponding author. Tel.: +1 212 2413194; fax: +1 212 9965787; e-mail: jing@msvax.mssm.edu.

Copyright © 1999 Elsevier Science Ltd. All rights reserved.

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Bladder Cancer-Sandalwood and Frankincense

http://www.ncbi.nlm.nih.gov/pubmed/25006348

Chin Med. 2014 Jul 2;9:18. doi: 10.1186/1749-8546-9-18. eCollection 2014.

Differential effects of selective frankincense (Ru Xiang) essential oil versus non-selective sandalwood (Tan Xiang) essential oil on cultured bladder cancer cells: a microarray and bioinformatics study.

Dozmorov MG1, Yang Q2, Wu W3, Wren J1, Suhail MM4, Woolley CL5, Young DG5, Fung KM6, Lin HK7.

Author information 

Abstract

BACKGROUND: 

Frankincense (Boswellia carterii, known as Ru Xiang in Chinese) and sandalwood (Santalum album, known as Tan Xiang in Chinese) are cancer preventive and therapeutic agents in Chinese medicine. Their biologically active ingredients are usually extracted from frankincense by hydrodistillation and sandalwood by distillation. This study aims to investigate the anti-proliferative and pro-apoptotic activities of frankincense and sandalwood essential oils in cultured human bladder cancer cells.

METHODS: 

The effects of frankincense (1,400-600 dilutions) (v/v) and sandalwood (16,000-7,000 dilutions) (v/v) essential oils on cell viability were studied in established human bladder cancer J82 cells and immortalized normal human bladder urothelial UROtsa cells using a colorimetric XTT cell viability assay. Genes that responded to essential oil treatments in human bladder cancer J82 cells were identified using the Illumina Expression BeadChip platform and analyzed for enriched functions and pathways. The chemical compositions of the essential oils were determined by gas chromatography-mass spectrometry.

RESULTS: 

Human bladder cancer J82 cells were more sensitive to the pro-apoptotic effects of frankincense essential oil than the immortalized normal bladder UROtsa cells. In contrast, sandalwood essential oil exhibited a similar potency in suppressing the viability of both J82 and UROtsa cells. Although frankincense and sandalwood essential oils activated common pathways such as inflammatory interleukins (IL-6 signaling), each essential oil had a unique molecular action on the bladder cancer cells. Heat shock proteins and histone core proteins were activated by frankincense essential oil, whereas negative regulation of protein kinase activity and G protein-coupled receptors were activated by sandalwood essential oil treatment.

CONCLUSION: 

The effects of frankincense and sandalwood essential oils on J82 cells and UROtsa cells involved different mechanisms leading to cancer cell death. While frankincense essential oil elicited selective cancer cell death via NRF-2-mediated oxidative stress, sandalwood essential oil induced non-selective cell death via DNA damage and cell cycle arrest.

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PMID:

 

25006348

 

[PubMed] 

PMCID:

 

PMC4086286

 

Bladder Cancer & Boswellia Carteri

BMC Complement Altern Med. 2009 Mar 18;9:6. doi: 10.1186/1472-6882-9-6.

Frankincense oil derived from Boswellia carteri induces tumor cell specific cytotoxicity.

Frank MB1, Yang Q, Osban J, Azzarello JT, Saban MR, Saban R, Ashley RA, Welter JC, Fung KM, Lin HK.

Author information 

Abstract

BACKGROUND: 

Originating from Africa, India, and the Middle East, frankincense oil has been important both socially and economically as an ingredient in incense and perfumes for thousands of years. Frankincense oil is prepared from aromatic hardened gum resins obtained by tapping Boswellia trees. One of the main components of frankincense oil is boswellic acid, a component known to have anti-neoplastic properties. The goal of this study was to evaluate frankincense oil for its anti-tumor activity and signaling pathways in bladder cancer cells.

METHODS: 

Frankincense oil-induced cell viability was investigated in human bladder cancer J82 cells and immortalized normal bladder urothelial UROtsa cells. Temporal regulation of frankincense oil-activated gene expression in bladder cancer cells was identified by microarray and bioinformatics analysis.

RESULTS: 

Within a range of concentration, frankincense oil suppressed cell viability in bladder transitional carcinoma J82 cells but not in UROtsa cells. Comprehensive gene expression analysis confirmed that frankincense oil activates genes that are responsible for cell cycle arrest, cell growth suppression, and apoptosis in J82 cells. However, frankincense oil-induced cell death in J82 cells did not result in DNA fragmentation, a hallmark of apoptosis.

CONCLUSION: 

Frankincense oil appears to distinguish cancerous from normal bladder cells and suppress cancer cell viability. Microarray and bioinformatics analysis proposed multiple pathways that can be activated by frankincense oil to induce bladder cancer cell death. Frankincense oil might represent an alternative intravesical agent for bladder cancer treatment.

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PMID:

 

19296830

 

[PubMed - indexed for MEDLINE] 

PMCID:

 

PMC2664784