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Biphenylalkylacetylhydroquinone ethers suppress the proliferation of murine B16 melanoma cells
Author(s) -
Fernandes Nicolle Valerie,
Jung Manfred,
Daoud Ali,
Mo Huanbiao
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1136.18
Subject(s) - chemistry , farnesol , cell growth , activator (genetics) , hydroquinone , apoptosis , cell cycle , cell cycle checkpoint , stereochemistry , pharmacology , biochemistry , biology , receptor
Hydroquinone, an activator of caspase‐9 activity via reactive oxygen species, and farnesol, a posttranslational down‐regulator of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase activity suppress the growth of murine B16 melanoma cells. Our previous studies have shown that farnesyl‐O‐acetylhydroquinone has a markedly greater growth‐suppressive activity than that predicted by the responses to the parent compounds. Perillyl alcohol, a modulator of small G‐protein activity, and biphenyl compounds, activators of Fas‐mediated death pathways, suppress B16 growth. A similar synergistic increase in the potency of each compound when ether‐linked to acetylhydroquinone is now reported. Perillyl‐O‐acetylhydroquinone, biphenylethyl‐O‐acetylhydroquinone and biphenylpropyl‐O‐acetylhydroquinone had dose‐dependent impacts on the proliferation of B16 cells with 50% inhibitory concentration (IC 50 ) values of 8.0, 4.2 and 1.4 μmol/L, respectively. The growth‐suppression effected by biphenylpropyl‐O‐acetylhydroquinone was accompanied by a dose‐dependent arrest at the G1/S interface of the cell cycle, an impact greater than that previously reported for farnesyl‐O‐acetylhydroquinone (IC 50 = 2.5 μmol/L). These new hydroquinone derivatives may have potential in cancer chemoprevention and/or therapy. TDA, TWU REP & Summer Stipend Award.