Cancer: Colorectal, prostate, gastric
Action: Anti-cancer
Apoptotic
Acetyl-keto-beta-boswellic acid (AKBA), a triterpenoid isolated from Boswellia carterri Birdw and Boswellia serrata, has been found to inhibit tumor cell growth and to induce apoptosis. Boswellic acids trigger apoptosis via a pathway dependent on caspase-8 activation, and independent of Fas/Fas ligand interaction in colon cancer HT-29 cells (Liu et al., 2002).
Colon Cancer
Although there is increasing evidence showing that boswellic acid might be a potential anti-cancer agent, the mechanisms involved in its action are unclear. It has been shown that acetyl-keto-beta-boswellic acid (AKBA) inhibits cellular growth in several colon cancer cell lines. Cell cycle analysis by flow cytometry showed that cells were arrested at the G1 phase after AKBA treatment.
These results demonstrate that AKBA inhibits cellular growth in colon cancer cells. These findings may have implications for the use of boswellic acids as potential anti-cancer agents in colon cancer (Liu et al., 2006).
AKBA significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell-cycle in G1-phase and induction of apoptosis. AKBA administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity (Yuan et al., 2013).
Gastric Cancer
AKBA exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited gastric cancer cells line SGC-7901 and MKN-45 xenografts without toxicity.
This effect might be associated with its roles in cell-cycle arrest and apoptosis induction. The results also showed activation of p21(Waf1/Cip1) and p53 in mitochondria and increased cleaved caspase-9, caspase-3, and PARP and Bax/Bcl-2 ratio after AKBA treatment. Upon AKBA treatment, β-catenin expression in nuclei was inhibited, and membrane β-catenin was activated (Zhang et al., 2013).
Prostate
The apoptotic effects and the mechanisms of action of AKBA were studied in LNCaP and PC-3 human prostate cancer cells. AKBA induced apoptosis in both cell lines at concentrations above 10 microg/mL. AKBA-induced apoptosis was correlated with the activation of caspase-3 and caspase-8 as well as with poly(ADP)ribose polymerase (PARP) cleavage.
AKBA treatment increased the levels of CAAT/enhancer binding protein homologous protein (CHOP) and activated a DR5 promoter reporter but did not activate a DR5 promoter reporter with the mutant CHOP binding site. These results suggest that AKBA induces apoptosis in prostate cancer cells through a DR5-mediated pathway, which probably involves the induced expression of CHOP (Lu et al., 2008).
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