Alpna Tyagi, PhD, of the University of Colorado Skaggs School of Pharmacy, and her team found that treatment with silibinin stopped the spread of these lung cancers in mouse.
Tissue with wound-like conditions allows tumours to grow and spread.
In the new animal study, silibinin help removed the molecular billboards that signal these wound-like conditions inhibiting the spread of these lung cancers,
Though the natural extract has been used for more than 2,000 years, mostly to treat disorders of the liver and gallbladder, this is one of the first carefully controlled and reported studies to find benefit.
Basically, in a cell there can be a chain of signals, one leading to the next, to the next, and eventually to an end product.
The end products COX2 and iNOS are enzymes involved with the inflammatory response to perceived wounds - both can aid tumour growth.
Far upstream in the signalling chain that leads to these unwanted enzymes are STAT1 and STAT3. These transcription factors allow the blueprint of DNA to bind with proteins that continue the signal cascade, eventually leading to the production of harmful COX2 and iNOS.
Stop STAT1 and STAT3 and you break the chain that leads to COX2 and iNOS - and the growth of lung tumours along with them.
"This relatively nontoxic substance - a derivative of milk thistle, called silibinin - was able to inhibit the upstream signals that lead to the expression of COX2 and iNOS," said Tyagi.
In addition, Tyagi and collaborators compared the effects of silibinin to drugs currently in clinical trials for lung cancer.
Compared to these multi-million dollar drugs, naturally occurring silibinin blocked not only the expression of COX2 and iNOS, but also the migration of existing lung cancer cells.
"What we showed is that STAT1 and STAT3 may be promising therapeutic targets in the treatment of lung cancer, no matter how you target them," Tyagi stated.
"And also that naturally-derived products like silibinin may be as effective as today's best treatments," she added.
The study has been recently published in the journal Molecular Carcinogenesis.