Hops, which contain compounds that add bitterness to beer, also contains a compound that brings bitter consequences to cancer cells, slowing their proliferation and even killing them outright. This cancer-killing compound, however, has a drawback. It is metabolized into a potent estrogen, one that poses serious health problems of its own.

The anticancer compound from hops is called xanthohumol (XL), and it has been modified by scientists at Oregon State University who hope to heighten its benefits while lowering its harms. According to these scientists, who were led by professor of biochemistry and biophysics Adrian Gombart, two XL derivatives might inspire drug developers to declare, thwarts cancer, less estrogen.

The scientists published their findings in an article (“Antiproliferative and Cytotoxic Activity of Xanthohumol and Its Non-Estrogenic Derivatives in Colon and Hepatocellular Carcinoma Cell Lines”) that appeared recently in the International Journal of Molecular Science.

“The XN derivatives dihydroxanthohumol (DXN) and tetrahydroxanthohumol (TXN) are not metabolized into 8-prenylnaringenin (8-PN), and they show higher tissue concentrations in vivo compared with XN when orally administered to mice at the same dose,” the article’s authors indicated. “Here we show that DXN and TXN possess improved anti-proliferative activity compared with XN in two colon (HCT116, HT29) and two hepatocellular (HepG2, Huh7) carcinoma cell lines, as indicated by their respective IC50 values.”

Earlier, Gombart’s colleague and co-author Fred Stevens led a study into DXN and TXN’s effects on metabolic syndrome.

“In that previous research we showed that the two derivatives reduced weight gain and improved biomarkers of metabolic syndrome,” Gombart said. “XN had been shown to inhibit proliferation of a variety of cancer cell lines, and in this study, we demonstrated XN’s ability to halt cell growth and kill two liver cancer cell lines and two colon cancer cell lines. We tested liver and colon cancer cell lines because oral consumption of XN and its derivatives can lead to high concentrations in the gut and liver.”

Colorectal cancer is the third most common cause of cancer-related death in the United States, and liver cancer ranks fifth. The incidence of liver cancer, though, has tripled in the last four decades.

XN, DXN, and TXN induce extensive apoptosis in all the carcinoma cell lines tested, the authors of the current study emphasized. They also reported that TXN induces G0/G1 cell cycle arrest in the colon carcinoma cell line HT29. “Our findings,” they wrote, “suggest that DXN and TXN could show promise as therapeutic agents against colorectal and liver cancer in preclinical studies without the drawback of metabolism into a phytoestrogen.”

“For both of those cancers, discovering new compounds for prevention and treatment is imperative,” Gombart concluded. “In all the cell lines tested, DXN and TXN inhibited cell growth and caused cell death, as did XN. And for most cell types, DXN and TXN were slightly more potent.”

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