The National Cancer Institute estimates that 1,685,210 new cases of cancer will be diagnosed in the US in 2016. Finding a cure has never been more urgent, and new research indicates that we may be one step closer.
A new study found that two drugs can mimic a common plant hormone and shut down the growth of certain cancer cells, according to a press release issued by Georgetown University Medical Center. The drugs caused DNA damage and turned off a major DNA repair mechanism in the cancer cells.
The two synthetic plant hormones are MEB55 and ST362, synthetic versions of strigolactones. Strigolactones are a class of plant hormone that regulates plant root and sprout growth.
Georgetown researchers have investigated the anti-cancer properties of plant hormones since 2009. They’ve conducted multiple studies showing that synthetic versions of strigolactones can stop cancer growth in breast, prostate, colon, lung and other tumor cells. This study looks at how, when combined with another cancer drug, these synthetic plant hormones can be lethal to prostate cancer cells.
“MEB55 and ST362 appear to be very promising agents," said senior investigator Ronit Yarden, PhD, in the press release."Our study suggests that when used with anti-cancer drugs called PARP inhibitors, the combination is effective and does not harm normal cells."
Yarden is assistant professor at the Georgetown University School of Nursing & Health Studies, as well as a member of the Georgetown Lombardi Comprehensive Cancer Center.
Yarden collaborated with researchers at the Agricultural Research Organization in Israel and the University of Turin, Italy, who first synthesized MEB55 and ST362. They were able to study the synthetic hormones in prostate cancer cells using a technique developed at Georgetown. The technique, called conditionally reprogrammed cells, allows cells to grow indefinitely.
The study found that whenever the synthetic hormones were combined with a PARP inhibitor (a cancer treatment drug), the cancer cells died. The synthetic plant hormones stopped the DNA repair process that happens after a cell replicates, and the PARP inhibitor shut down a second repair pathway. The cancer cells had no alternative, but to die.
“Mistakes in copying DNA are especially prevalent in cancer cells, so without any way to repair their DNA, these cells self destruct,” said Yarden in the press release.
She hopes to soon test the combination in animals and on various types of cancer.
The full study was published in Oncotarget. The research was funded in part by the National Institutes of Health and Georgetown University.
The authors disclosed no conflicts of interest.
