Recently, scientists demonstrated the anti-cancer effects of silibinin, a major biologically active compound of milk thistle. Being widely used as a folk remedy for liver diseases, milk thistle is safe and well-tolerated, and it protects the liver from drug or alcohol-related injury. Silibinin is highly purified from milk thistle, with a defined chemical structure and molecular weight (C25H22O10, MW: 482.44).
The study was carried out by Dr. Ke-Qin Hu and his research team at the University of California, Irvine. Dr. Hu is a long�Cterm and well-experienced research scientist and physician in the field of hepatology. He has published over 70 scientific articles in various medical professional journals. Many of his scientific research publications are focused on viral hepatitis B and C, cirrhosis, and liver cancer, all of which have significantly contributed to our better understanding of common liver diseases.
Dr. Hu and his colleagues' discovery of silibilin�'s anti-liver cancer effects was published in the October 28 issue of the World Journal of Gastroenterology.
The researchers found that silibilin can significantly reduce the growth of several human hepatoma cell lines. In addition, they demonstrated that silibinin mediates anti-liver cancer effects by (1) reduced cancer cell proliferation and cell cycle progression; (2) enhanced programmed death of cancer cells; and (3) altered chromatin structure of the cancer cells.
Their research results indicate that silibinin can be used to prevent the development of liver cancer, one of the most common cancers worldwide. The results have also opened our minds to the possibility of testing other herbal supplements for possible treatment of human cancers.
Investigators publish new data in the report 'Silibinin impairs constitutively active TGFalpha-EGFR autocrine loop in advanced human prostate carcinoma cells.'
According to recent research from the United States, "Epidermal growth factor (EGF) and transformation growth factor-alpha (TGFalpha) are potent mitogens that regulate proliferation of prostate cancer cells via autocrine and paracrine loops, and promote tumor metastasis. They exert their action through binding to the cell surface receptor, epidermal growth factor receptor (EGFR), and cause activation of Erk1/2 mediated mitogenic signaling in human prostate cancer (PCA) at both advanced and androgen-independent stages."
"Thus, we rationalized that inhibiting this mitogenic pathway could be useful in controlling advanced PCA growth. LNCaP and DU145 human PCA cells were treated with silibinin (100-200 microM) for different time points, and the levels of TGFalpha, activated signaling molecules (EGFR, Erk1/2 and Jnk1/2) and Erk1/2 kinase activity were analyzed employing ELISA, immunoprecipitation and/or immunoblotting techniques. The mRNA levels of TGFalpha were analyzed by RT-PCR.
Treatment of cells (LNCaP and DU145) with silibinin resulted in a decrease in TGFalpha protein at both secreted and cellular levels together with a decrease in its mRNA level. Silibinin also caused an inhibition of EGFR activation followed by that of Erk1/2 without any change in their protein levels. The kinase activity of Erk1/2 to Elk1 was also inhibited by silibinin at least in DU145 cells.
In other study, silibinin caused strong inhibition of Jnk1/2 activation in LNCaP cells while in DU145 cells, a strong induction in Jnk1/2 activation was observed. These results suggest that silibinin impairs TGFalpha-EGFR-Erk1/2 signaling in both androgen-dependent (LNCaP) and -independent (DU145) advanced human prostate carcinoma cells," wrote A. Tyagi and colleagues, University of Colorado, Department of Pharmaceutical Sciences (see also Prostate Cancer Immunology).
The researchers concluded: "This study, for the first time, identifies the inhibitory effect of silibinin on constitutively active TGFalpha-EGFR autocrine loop in advanced human PCA cells, which plausible contributes to the strong efficacy of silibinin in PCA prevention and intervention, as reported in recent studies."
Tyagi and colleagues published their study in Pharmaceutical Research (Silibinin impairs constitutively active TGFalpha-EGFR autocrine loop in advanced human prostate carcinoma cells. Pharmaceutical Research, 2008;25(9):2143-50).