Lin X, Switzer B R, Demark-Wahnefried W
Division of Urologic Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Anticancer Res. 2001 Nov-Dec;21(6A):3995-9.
Mammalian lignans, enterolactone (EL) and enterodiol (ED), have been shown to inhibit breast and colon carcinoma. To date, there have been no reports of the effect of lignans on prostatic carcinoma. We investigated the effects of ED and EL on three human prostate cancer cell lines (PC-3, DU-145 and LNCaP).
Cells were treated with either 0.1% (v/v) DMSO (vehicle) or 10-100 microM of EL, ED or genistein (positive control) for 72 hours. Cell viability was measured by the propidium iodide nuclei staining fluorometric assay with each assay performed in triplicate.
At 10-100 microM, EL significantly inhibited the growth of all cell lines, whereas ED only inhibited PC-3 and LNCaP cells. While EL was a more potent growth inhibitor than ED, both were less potent than genistein. The dose for 50% growth inhibition of LNCaP cells (IC50) by EL was 57 microM, whereas IC50 was 100 microM for ED, (the observed IC50 for genistein was 25 microM).
ED and EL suppress the growth of prostate cancer cells, and may do so via hormonally-dependent and independent mechanisms.
哺乳动物木脂素，肠内酯（EL）和肠二醇（ED），已被证明可抑制乳腺癌和结肠癌。迄今为止，尚无关于木脂素对前列腺癌作用的报道。我们研究了ED和EL对三种人前列腺癌细胞系（PC-3、DU-145和LNCaP）的影响。
细胞用0.1%（v/v）二甲基亚砜（溶剂）或10 - 100微摩尔的EL、ED或染料木黄酮（阳性对照）处理72小时。通过碘化丙啶细胞核染色荧光测定法测量细胞活力，每次测定重复三次。
在10 - 100微摩尔浓度下，EL显著抑制所有细胞系的生长，而ED仅抑制PC-3和LNCaP细胞。虽然EL是比ED更有效的生长抑制剂，但两者都不如染料木黄酮有效。EL对LNCaP细胞50%生长抑制的剂量（IC50）为57微摩尔，而ED的IC50为100微摩尔，（观察到染料木黄酮的IC50为25微摩尔）。
ED和EL抑制前列腺癌细胞的生长，并且可能通过激素依赖性和非依赖性机制实现。
