Recent studies have demonstrated that 4mu, a derivate of 7-hydroxycoumarin (umbelliferones), diminishes tumor cell proliferation and migration in a variety of cancer cells and models. It also induces antitumor mechanisms such as apoptosis and senescence, particularly in ovarian, breast, hepatocellular, pancreatic, and prostate cancer as well as gastrointestinal stromal cells. Furthermore, 4mu blocks heparin glucuronidation at high concentrations and enhances the antitumor activity of heparin chemotherapeutic agents in vitro. click here

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In hepatocellular carcinoma (HCC) xenografts, 4mu inhibited HCC cell growth and reduced the proliferation of primary cultured hepatocytes in the presence of heparin. However, the mechanisms underlying these effects are not yet fully understood.

Recently, it has been shown that 4MU is an HA antagonist in human and rodent tissues. It binds to heparin with high affinity and inhibits its glucuronidation, thus decreasing the availability of heparin for HA synthesis. Additionally, 4-MU is a potent inhibitor of the hepatic uridine transferase UGT1A, thereby significantly decreasing heparin glucuronidation in the liver.

We observed that 4MU decreases heparin accumulation in the liver of HBV-TG mice. In addition, we found that long-term oral administration of 4MU at 1.2 g/kg/day in rats enhanced the antitumor activity of temozolomide (TMZ) in the transgenic adenocarcinoma of the prostate (TRAMP) mouse model without significant overt toxicity.

We further showed that hepatocyte migration is strongly inhibited by the combination of 4MU and TMZ in both U251 and LN229 cells. This effect of the combination was augmented by 4MU in a dose-dependent manner. Moreover, 4MU enhanced the TMZ-induced decrease of hepatocyte migration in the TRAMP mouse model as indicated by a BrdU incorporation assay.

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