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Geranylgeraniol suppresses the proliferation of murine melanoma cells and human prostate tumor cells

The rate‐limiting activity of the mevalonate pathway, 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG CoA) reductase, provides essential intermediates for the prenylation or dolichylation of growth‐related proteins including nuclear lamins, Ras and growth factor receptors. A diterpene geranylgeraniol accelerates HMG CoA reductase degradation and suppresses the growth of human liver, lung, ovary, pancreas, colon, stomach, and blood tumors. We evaluated geranylgeraniol in murine and human cells. Geranylgeraniol induced dose‐dependent suppression of the cell proliferation following 48 (murine B16 melanoma) or 72 (human DU145 prostate carcinoma) h incubations in 96‐well plates. Cell cycle arrest at the G1 phase, manifested by a dose‐dependent increase in G1/S ratio, and apoptosis detected by fluorescence microscopy following acridine orange and ethidium bromide dual staining, contribute to the growth suppression in DU145 cells. The impact of geranylgeraniol on B16 cell proliferation was attenuated by supplemental mevalonate. Geranylgeraniol also attenuated the growth of human LNCaP prostate carcinoma and PC‐3 prostate adenocarcinoma cells. Mouse 3T3‐L1 fibroblasts were more resistant than B16 cells to geranylgeraniol. The differential sensitivity between neoplastic and normal cells points to the potential application of geranylgeraniol to cancer prevention. TDA, TWU REP & Summer Stipend Award.