Milk thistle extract stops lung cancer in mice

November 15, 2011

Tissue with wound-like conditions allows tumors to grow and spread. In mouse lung cancer cells, treatment with silibinin, a major component of milk thistle, removed the molecular billboards that signal these wound-like conditions and so stopped the spread of these lung cancers, according to a recent study published in the journal Molecular Carcinogenesis.

Though the natural extract has been used for more than 2,000 years, mostly to treat disorders of the liver and , this is one of the first carefully controlled and reported studies to find benefit.

Here is how it works:

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. And so if you would like to eliminate an end product, you may look to break a link in the signaling chain that leads to it. The end products and iNOS are enzymes involved with the to perceived wounds – both can aid growth. Far upstream in the signaling 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 tumors 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," says Alpna Tyagi, PhD, investigator at the University of Colorado Cancer Center and member of the Agarwal Lab at the Skaggs School of Pharmacy and Pharmaceutical Sciences.

In addition, Tyagi and collaborators compared the effects of silibinin to drugs currently in clinical trials for lung cancer. Would drugs that target other signaling pathways – other linked chains – similarly cut into the production of COX2 and iNOS?

It turned out that inhibiting the chains of JAK1/2 and MEK in combination and also inhibiting the signaling pathways of EGFR and NF-kB in combination blocked the ability of STAT1 and STAT3 to trap the energy they needed to eventually signal COX2 and iNOS production.

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 .

"What we showed is that STAT1 and STAT3 may be promising therapeutic targets in the treatment of , no matter how you target them," Tyagi says. "And also that naturally-derived products like silibinin may be as effective as today's best treatments."

Explore further: Reversing smoke-induced damage and disease in the lung

Related Stories

Reversing smoke-induced damage and disease in the lung

October 13, 2011
By studying mice exposed to tobacco smoke for a period of months, researchers have new insight into how emphysema and chronic obstructive pulmonary disease (COPD) develops. In the October 14th issue of Cell they also report ...

New study finds compounds show promise in blocking STAT3 signaling as treatment for osteosarcoma

April 11, 2011
A study appearing in the journal Investigational New Drugs and conducted by researchers at Nationwide Children's Hospital, discovered that two new small molecule inhibitors are showing promise in blocking STAT3, a protein ...

New drug target for kidney disease discovered

April 26, 2011
Two discoveries at UC Santa Barbara point to potential new drug therapies for patients with kidney disease. The findings are published in this week's issue of the Proceedings of the National Academy of Sciences.

TGen presents lung cancer studies at Amsterdam conference

July 7, 2011
The Translational Genomics Research Institute (TGen) is presenting two key studies, including one today, at the 14th World Conference on Lung Cancer, July 3-7 in Amsterdam.

Recommended for you

Cancer-death button gets jammed by gut bacterium

July 27, 2017
Researchers at Michigan Medicine and in China showed that a type of bacterium is associated with the recurrence of colorectal cancer and poor outcomes. They found that Fusobacterium nucleatum in the gut can stop chemotherapy ...

Researchers release first draft of a genome-wide cancer 'dependency map'

July 27, 2017
In one of the largest efforts to build a comprehensive catalog of genetic vulnerabilities in cancer, researchers from the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute have identified more than 760 genes ...

Long-sought mechanism of metastasis is discovered in pancreatic cancer

July 27, 2017
Cells, just like people, have memories. They retain molecular markers that at the beginning of their existence helped guide their development. Cells that become cancerous may be making use of these early memories to power ...

Blocking the back-door that cancer cells use to escape death by radiotherapy

July 27, 2017
A natural healing mechanism of the body may be reducing the efficiency of radiotherapy in breast cancer patients, according to a new study.

Manmade peptides reduce breast cancer's spread

July 27, 2017
Manmade peptides that directly disrupt the inner workings of a gene known to support cancer's spread significantly reduce metastasis in a mouse model of breast cancer, scientists say.

Glowing tumor technology helps surgeons remove hidden cancer cells

July 27, 2017
Surgeons were able to identify and remove a greater number of cancerous nodules from lung cancer patients when combining intraoperative molecular imaging (IMI) - through the use of a contrast agent that makes tumor cells ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.