Pigment Found in Chamomile, Parsley Kills Mesothelioma Cells
A yellowish pigment common to parsley, celery, chamomile tea, oranges and grapefruit may be the latest treatment for mesothelioma cancer, a new study shows.
While numerous studies have demonstrated the anti-cancer and antioxidant properties of apigenin (API), the natural pigment found in these plants and vegetables, researchers recently tested it against malignant mesothelioma cells.
Doctors at the University of Rome evaluated the anti-tumor activities of API in mice injected with mesothelioma cells.
API inhibited malignant mesothelioma (MM) cell survival and activated cell death, known as apoptosis. Mice treated with API survived nearly twice as long as the control mice, underlining the compound’s potential for future research and clinical trials.
“We demonstrated for the first time that API treatment was able to inhibit the growth of MM cell lines in vivo,” lead researcher Dr. Laura Masuelli wrote in the study. “Overall, we demonstrated that Apigenin inhibited in vitro and in vivo malignant mesothelioma cells growth by targeting different signaling pathways and inducing apoptosis.”
Apigenin Lessened Fluid Buildup in Mice
Lab mice implanted with MM cells experienced abnormal fluid buildup in their abdominal cavity.
Injecting API directly into the abdomen (intraperitoneal injections) improved the condition and increased the median survival of the mice.
Peritoneal mesothelioma is the second-most-common type of the asbestos-related cancer. Tumors form on the peritoneum, which is the protective membrane that surrounds the abdomen.
Currently, the best traditional treatment for peritoneal mesothelioma is a combination of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (HIPEC), where heated chemotherapy drugs are delivered directly to the abdominal cavity after surgery attempts to remove as much cancerous growth as possible.
Adding a natural compound, such as apigenin, to the mix may increase the effects of HIPEC and other traditional therapies.
Pleural mesothelioma, which forms on the lining of the lungs, is the most common type of the asbestos-related disease. Scientists around the world are exploring heated chemotherapy, immunotherapy, gene therapy and other emerging therapies as options for directly treating pleural mesothelioma as well.
“The local administration of drugs in the peritoneal or pleural space might be an improved strategy to treat MM,” Masuelli wrote.
Apigenin Benefits & Drawbacks
Apigenin belongs to the chemical compound class of polyphenols, which have the ability to modify the activity of multiple targets involved in carcinogenesis through direct interaction or modulation of gene expression.
Researchers discovered apigenin caused cell death of mesothelioma cells by:
- Increasing the ratio between Bax and Bcl-2 proteins
- Raising expression of p53, a gene that codes for a protein that regulates the cell cycle and acts as a tumor suppressor
- Activating certain enzymes (caspase 9 and caspase 8)
- Causing cell division of the PARP-1 enzyme
- Increasing the percentage of cells measurable by the sub-G1 assay
While API induced apoptosis in mesothelioma cells, it did not trigger autophagy, which is the destructive mechanism of the cell that disassembles unnecessary or dysfunctional components.
Still, the compound showed a significant survival increase in lab mice, who were euthanized at the first signs of distress. All control mice were euthanized at five or six weeks, while API-treated mice survived nine to 12 weeks.
“Overall, when comparing the survival of mice upon treatment, it was observed that API treatment prolonged mice median survival time as compared to the vehicle treatment,” Masuelli wrote. “Our results indicated that API specifically interfered with intraperitoneally transplanted [malignant mesothelioma] cell growth.”
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1 Cited Article Sources
- Masuelli, L. et al. (2017, June 19). In Vitro and In Vivo Anti-tumoral Effects of the Flavonoid Apigenin in Malignant Mesothelioma. Retrieved from: http://journal.frontiersin.org/article/10.3389/fphar.2017.00373/full