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Respiratory activities of PrEC cell mitochondria were 5-20-fold lower than PC mitochondria, depending on substrates and the metabolic state, due to lower content and lower activity of the respiratory enzyme complexes. PrEC cells contained 2 to 4 times less mitochondria per gram of cells than the three PC cell lines. We studied mitochondria isolated from normal prostate epithelial cells (PrEC, metastatic prostate cancer cell lines LNCaP, PC-3, DU 145 and non-prostate cancer cells - human fibrosarcoma HT1080 cells and normal human lymphoblastoid cells. Copyright 2000 Wiley-Liss, Inc.īioenergetic and antiapoptotic properties of mitochondria from cultured human prostate cancer cell lines PC-3, DU 145 and LNCaP.ĭirectory of Open Access Journals (Sweden)įull Text Available The purpose of this work was to reveal the metabolic features of mitochondria that might be essential for inhibition of apoptotic potential in prostate cancer cells. These results suggest that LNCaP and DU 145 prostate cancer cells show differences not only in androgen responsiveness but in sensitivity to taxol as well. Simultaneous treatment with R1881 and taxol had no additional effects on LNCaP or DU 145 cells.
Additional taxol effects were seen in DU 145 cells with micronucleation of DNA, an indication of apoptosis. Treatment with taxol resulted in bundling of microtubules in both cell lines. As expected, the androgen-independent prostate cancer cell line DU 145 was not affected by R1881. The effects of taxol included microtubule bundling and altered mitochondria morphology, but not DNA organization. Microtubules were only faintly detected in 1 nM R1881-treated LNCaP cells. Although centrosomes were closely associated with the nucleus in untreated cells, they dispersed into the cytoplasm after treatment with 1 nM R1881. Immunofluorescence microscopy with antibodies to centrosomes showed altered centrosome structure. After treatment with 1 nM R1881, chromatin became clustered, nuclear envelopes convoluted, and mitochondria accumulated around the nucleus. Treatment of LNCaP cells with 0.05 nM R1881 led to increased cell proliferation, whereas treatment with 1 nM R1881 resulted in inhibited cell division, DNA cycle arrest, and altered centrosome organization. Cells were treated for 48 and 72 h with 0.05-1 nM of the synthetic androgen R1881 and with 100 nM taxol. We investigated the effects of androgen and taxol on the androgen-responsive LNCaP and androgen-independent DU 145 prostate cancer cell lines. Androgen and taxol cause cell type-specific alterations of centrosome and DNA organization in androgen-responsive LNCaP and androgen-independent DU 145 prostate cancer cells
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