Isolation of a human prostate carcinoma cell line (DU 145)

Stone, Kevin; Mickey, Don D.; Wunderli, Heidi; Mickey, George H.; Paulson, David F.

doi:10.1002/ijc.2910210305

Cited by 1,012 publications

(610 citation statements)

References 22 publications

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“…The cell line DU-145 was originally derived from a brain metastasis of a human prostate adenocarcinoma (Stone et al, 1978); it retains the androgen independence of the original tumour and does not express a functional androgen receptor . This cell line possesses both LHRH and EGF receptors and produces EGFR ligands TGF-a and EGF (Xie et al, 1995;Jungwirth et al, 1997a).…”

Section: Du-145 Cell Linesmentioning

confidence: 99%

Luteinising hormone-releasing hormone analogue reverses the cell adhesion profile of EGFR overexpressing DU-145 human prostate carcinoma subline

2005

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Cetrorelix, a luteinising hormone-releasing hormone (LHRH) analogue, has been shown to limit growth of the human androgenindependent prostate cell line DU-145, although other inhibitory actions may also be affected. Both growth and invasion of DU-145 cells are linked to autocrine epidermal growth factor receptor (EGFR) signalling. Invasiveness requires not only cells to migrate to conduits, but also reduced adhesiveness between tumour cells to enable separation from the tumour mass. Thus, we investigated whether Cetrorelix alters the DU-145 cell -cell adhesion and if this occurs via altered EGFR signalling. Pharmacologic levels of Cetrorelix limited the invasiveness of a highly invasive DU-145 subline overexpressing full-length EGFR (DU-145 WT). Extended exposure of the cells to Cetrorelix resulted in increased levels of the cell -cell adhesion complex molecules E-cadherin, a-and bcatenin, and p120. Puromycin blocked the increases in E-cadherin and b-catenin levels, suggesting that de novo protein synthesis is required. The Cetrorelix effect appears to occur via transmodulation of EGFR by a protein kinase C (PKC)-dependent mechanism, as there were no changes in DU-145 cells expressing EGFR engineered to negate the PKC transattenuation site (DU-145 A654); downregulation of EGFR signalling produced a similar upregulation in adhesion complex proteins, further suggesting a role for autocrine signalling. Cetrorelix increased the cell -cell adhesiveness of DU-145 WT cells to an extent similar to that seen when autocrine EGFR signalling is blocked; as expected, DU-145 A654 cell -cell adhesion also was unaffected by Cetrorelix. The increased adhesiveness is expected as the adhesion complex molecules moved to the cells' periphery. These data offer direct insight into the possible crosstalk pathways between the LHRH and EGFR receptor signalling. The ability of Cetrorelix to downregulate EGFR signalling and subsequently reverse the antiadhesiveness found in metastatic prostate cancer highlights a novel potential target for therapeutic strategies.

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Section: Du-145 Cell Linesmentioning

confidence: 99%

Luteinising hormone-releasing hormone analogue reverses the cell adhesion profile of EGFR overexpressing DU-145 human prostate carcinoma subline

2005

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“…The LNCaP and DU145 cell lines were originally isolated from metastatic lesions of patients suffering from prostate cancer (Stone et al, 1978;Horoszewicz et al, 1983) and purchased from DSMZ (Braunschweig, Germany) as American Type Culture Collection (ATCC) cell lines. HeLa cells were derived from a cervical carcinoma (Scherer et al, 1953) obtained from Dr Aubee.…”

Section: Cell Lines and Culture Conditionsmentioning

confidence: 99%

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

2003

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Nine human tumour cell lines (four mammary, one bladder, two prostate, one cervical, and one squamous cell carcinoma) were studied as to whether cellular radiosensitivity is related to the number of initial or residual double-strand breaks (dsb). Cellular sensitivity was measured by colony assay and dsb by means of constant-and graded-field gel electrophoresis (CFGE and GFGE, respectively). The nine tumour cell lines showed a broad variation in cellular sensitivity (SF2 0.17 -0.63). The number of initial dsb as measured by GFGE ranged between 14 and 27 dsb/Gy/diploid DNA content. In contrast, normal fibroblasts raised from skin biopsies of seven individuals showed only a marginal variation with 18 -20 dsb/Gy/diploid DNA content. For eight of the nine tumour cell lines, there was a significant correlation between the number of initial dsb and the cellular radiosensitivity. The tumour cells showed a broad variation in the amount of dsb measured 24 h after irradiation by CFGE, which, however, was not correlated with the cellular sensitivity. This residual damage was found to be influenced not only by the actual number of residual dsb, but also by apoptosis and cell cycle progression which had impact on CFGE measurements. Some cell line strains were able to proliferate even after exposure to 150 Gy while others were found to degrade their DNA. Our results suggest that for tumour cells, in contrast to normal cells, the variation in sensitivity is mainly determined by differences in the initial number of dsb induced.

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“…38 Two androgennonresponsive cell lines were used: PC3 cells were derived from a human prostatic adenocarcinoma metastatic to the bone, 39 and DU-145 prostate carcinoma cells were derived from a human prostate adenocarcinoma metastatic to the brain. 40 LNCaP, DU-145, and PC3 cells were grown in DMEM supplemented with 30 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES), 10% FBS, 60 units/mL penicillin, and 60 units/mL streptomycin. The MDA-PCa-2b cells were cultured in Kaighn-modified Ham F12 medium with 2 mM L-glutamine that was modified by the ATCC to contain 1.5 g/L sodium bicarbonate.…”

Section: Cell Culturementioning

confidence: 99%

Indole‐3‐carbinol induces a G1 cell cycle arrest and inhibits prostate‐specific antigen production in human LNCaP prostate carcinoma cells

Zhang

Hsu

Kinseth

et al. 2003

Cancer

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BACKGROUNDIndole‐3‐carbinol (I3C), a naturally occurring component of Brassica vegetables, such as cabbage, broccoli, and Brussels sprouts, is a promising anticancer agent for certain reproductive tumor cells. The objective of the current study was to characterize the cell cycle effects of I3C in human prostate carcinoma cells.METHODSThe incorporation of [3H]thymidine and flow cytometry of propidium iodide–stained nuclei were used to monitor I3C‐regulated changes in prostate carcinoma cell proliferation and cell cycle progression. Western blotting was used to document expression changes in cell cycle components and prostate‐specific antigen (PSA) levels. The enzymatic activities of cyclin‐dependent kinases (CDK) were tested by in vitro protein kinase assays using the retinoblastoma protein as a substrate.RESULTSI3C suppressed the growth of LNCaP prostate carcinoma cells in a dose‐dependent manner by inducing a G1 block in cell cycle progression. I3C selectively inhibited the expression of CDK6 protein and transcripts and strongly stimulated the production of the p16 CDK inhibitor. In vitro protein kinase assays revealed the striking inhibition by I3C of immunoprecipitated CDK2 enzymatic activity and the relatively minor down‐regulation of CDK4 enzymatic activity. In LNCaP prostate carcinoma cells, I3C treatment inhibited production of PSA, whereas combinations of I3C and the androgen antagonist flutamide more effectively inhibited DNA synthesis and PSA levels compared with either agent alone.CONCLUSIONSThe results of the current study demonstrated that I3C has a potent antiproliferative effect in LNCaP and other human prostate carcinoma cells. These findings implicate this dietary indole as a potential chemotherapeutic agent for controlling the growth of human prostate carcinoma cells. Cancer 2003. © 2003 American Cancer Society.

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Isolation of a human prostate carcinoma cell line (DU 145)

Cited by 1,012 publications

References 22 publications

Luteinising hormone-releasing hormone analogue reverses the cell adhesion profile of EGFR overexpressing DU-145 human prostate carcinoma subline

Luteinising hormone-releasing hormone analogue reverses the cell adhesion profile of EGFR overexpressing DU-145 human prostate carcinoma subline

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

Indole‐3‐carbinol induces a G1 cell cycle arrest and inhibits prostate‐specific antigen production in human LNCaP prostate carcinoma cells

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