Cells age and die as part of their natural cycle. Cancer cells, despite being an altered version of a cell, can have the same life cycle. The key is finding out how to make them age and die without harming healthy tissues around them.

This cellular study focused on the effects of a compound from Boswellia serrata called acetyl-11-keto-beta-boswellic acid, known as “AKBA” on hepatocellular carcinoma cells – the most common form of liver cancer. According to the Mayo Clinic, it typically affects individuals with hepatitis B or C.

The researchers found that low levels of AKBA interrupted the cell growth cycle of liver cancer cells. It also prevented the cells’ DNA repair response, prematurely “aging” the cell in order to kill it.

In some ways, this isn’t a surprise. AKBA is one of boswellia’s most valuable components, helping fight everything from asthma to rheumatoid arthritis because of its ability to stop 5-lipooxygenase (5-LOX) inflammation. Other work has found that boswellia extracts with higher levels of AKBA also help to kick in the body’s own defenses to stop tumors from growing.

But is important to bear in mind that while AKBA is naturally present in boswellia, that any supplemental form should be standardized for enhanced levels of the compound – at least to 10 percent or more. Also, boswellia contains another compound called “beta-boswellic acid” that can actually be pro-inflammatory. Be certain to look for boswellia that is standardized to reduce levels of beta-boswellic acid, while preserving higher levels (but not overly spiked levels) of AKBA for the best results.

Abstract:

Wang S, Wang H, Sun B, et al.  Acetyl-11-keto-β-boswellic acid triggers premature senescence via induction of DNA damage accompanied by impairment of DNA repair genes in hepatocellular carcinoma cells in vitro and in vivo. Fundam Clin Pharmacol. 2019 May 29.

Cellular senescence, a state of irreversible growth arrest, occurs in all somatic cells and causes the cells to exhaust replicative capacity. Recently, cellular senescence has been emerging as one of the principal mechanisms of tumor suppression, which can be induced by low doses of therapeutic drugs in cancer cells. Acetyl-11-keto-β-boswellic acid (AKBA), an active ingredient isolated from the plant Boswellia serrata, has been identified to induce apoptosis in hepatocellular carcinoma (HCC) cells. In this study, we found that low concentrations of AKBA treatment triggered cell growth arrest at G0/G1 phase with features of premature cellular senescence phenotype in both HCC cell lines HepG2 and SMMC7721, as observed by enlarged and flattened morphology, significant increase in cells with senescence-associated β-galactosidase staining, and decrease in cell proliferation and DNA synthesis. Furthermore, cellular senescence induced by AKBA occurred via activation of DNA damage response and impairment of DNA repair, as evidenced by strong induction of γH2AX and p53, and downregulated expressions of multiple DNA repair associated genes. Induction of p53 by AKBA caused a significant increase in p21CIP1 , which had a critical involvement in the induction of cellular senescence. Additionally, in vivo study demonstrated that induction of senescence contributed to the anticancer efficacy of AKBA. Therefore, our findings suggested that induction of premature senescence by AKBA through DNA damage response accompanied by impairment of DNA repair genes defines a novel mechanism contributing to its growth suppression in HCC cells.