Fatty acid composition of phospholipids in epithelium and stroma of human benign prostatic hyperplasia

Weisser, Heike; Krieg, Michael

doi:10.1002/(sici)1097-0045(19980901)36:4<235::aid-pros4>3.0.co;2-e

Cited by 22 publications

(7 citation statements)

References 30 publications

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“…Phosphatidic acid is also implicated in cell motility associated with metastasis ( Mazie et al , 2006 ; Clarke et al 2009 ). Fatty acids in PtdOH derived from PtdEtn will be more unsaturated than those from PtdCho ( Pettitt et al 1997 ; Weisser and Krieg 1998 ) while PtdOH from PlasEtn will contain 1- 0 -alkyl or 1- 0 -alkenyl chains. Such structural differences may result in EtnPG-derived PtdOH having different signalling, protein interaction, membrane fusion and fission properties, all linked to tumorigenesis ( Jenkins and Frohman 2005 ; Wang et al , 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Phorbol ester stimulates ethanolamine release from the metastatic basal prostate cancer cell line PC3 but not from prostate epithelial cell lines LNCaP and P4E6

et al. 2014

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Background:Malignancy alters cellular complex lipid metabolism and membrane lipid composition and turnover. Here, we investigated whether tumorigenesis in cancer-derived prostate epithelial cell lines influences protein kinase C-linked turnover of ethanolamine phosphoglycerides (EtnPGs) and alters the pattern of ethanolamine (Etn) metabolites released to the medium.Methods:Prostate epithelial cell lines P4E6, LNCaP and PC3 were models of prostate cancer (PCa). PNT2C2 and PNT1A were models of benign prostate epithelia. Cellular EtnPGs were labelled with [1-3H]-Etn hydrochloride. PKC was activated with phorbol ester (TPA) and inhibited with Ro31-8220 and GF109203X. D609 was used to inhibit PLD (phospholipase D). [3H]-labelled Etn metabolites were resolved by ion-exchange chromatography. Sodium oleate and mastoparan were tested as activators of PLD2. Phospholipase D activity was measured by a transphosphatidylation reaction. Cells were treated with ionomycin to raise intracellular Ca2+ levels.Results:Unstimulated cell lines release mainly Etn and glycerylphosphorylEtn (GPEtn) to the medium. Phorbol ester treatment over 3h increased Etn metabolite release from the metastatic PC3 cell line and the benign cell lines PNT2C2 and PNT1A but not from the tumour-derived cell lines P4E6 and LNCaP; this effect was blocked by Ro31-8220 and GF109203X as well as by D609, which inhibited PLD in a transphosphatidylation reaction. Only metastatic PC3 cells specifically upregulated Etn release in response to TPA treatment. Oleate and mastoparan increased GPEtn release from all cell lines at the expense of Etn. Ionomycin stimulated GPEtn release from benign PNT2C2 cells but not from cancer-derived cell lines P4E6 or PC3. Ethanolamine did not stimulate the proliferation of LNCaP or PC3 cell lines but decreased the uptake of choline (Cho).Conclusions:Only the metastatic basal PC3 cell line specifically increased the release of Etn on TPA treatment most probably by PKC activation of PLD1 and increased turnover of EtnPGs. The phosphatidic acid formed will maintain a cancer phenotype through the regulation of mTOR. Ethanolamine released from cells may reduce Cho uptake, regulating the membrane PtdEtn:PtdCho ratio and influencing the action of PtdEtn-binding proteins such as RKIP and the anti-apoptotic hPEBP4. The work highlights a difference between LNCaP cells used as a model of androgen-dependent early stage PCa and androgen-independent PC3 cells used to model later refractory stage disease.

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Section: Discussionmentioning

confidence: 99%

Phorbol ester stimulates ethanolamine release from the metastatic basal prostate cancer cell line PC3 but not from prostate epithelial cell lines LNCaP and P4E6

et al. 2014

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“…The recent work of Weisser and Krieg [72] demonstrated the existence of the proposed difference in membrane lipid composition between epithelium and stroma of human BPH, and that the patterns seen in the two compartments evolve with age and, as a consequence, in their endogenous hormonal milieu. In particular, the percentage of oleic acid is higher and the AA concentration is lower in epithelium than in stroma.…”

Section: Source Of Lipidsmentioning

confidence: 99%

“…Fatty acid concentration is higher in epithelium than in stroma, is more unsaturated, and decreases significantly with age. Because an increase both in chain length and in ratio of saturated to unsaturated fatty acids is found in the stroma, Weisser and Krieg [72] concluded that the stromal membrane(s) is more rigid, i.e., less fluid, than that of the epithelium. They further believed that the significant difference in lipid composition between epithelium and stroma, as well as the age-dependent changes, supported their hypothesis that lipids and, by inference, Prl, are somehow involved in the modulation of 5␣-reductase activity.…”

Section: Source Of Lipidsmentioning

confidence: 99%

Estrogen in the etiopathogenesis of BPH

Farnsworth

1999

Prostate

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BACKGROUND While the androgen‐dependence of the prostate gland has long been accepted, the participation of estrogen, mediated via the stroma in the elicitation of benign prostatic hyperplasia (BPH), has only recently been recognized. Its mode of action is still uncertain. METHODS This review first outlines the regulation of gene expression via hormones, growth factors, and other ligands in the coordination of cell growth, differentiation, and function. Focus is next directed to factors particularly involved in phosphorylation of estrogen receptors. Then, the access of sex steroids, especially of estrogen to the cell and to the transduction machinery, is described, preparatory to examining the hypotheses by which this access causes the process of BPH to occur. RESULTS It becomes clear that the necessary phosphorylative activities which transmit signals to nuclear receptors and thence transcription of target genes can be performed by steroids or mimicked by proxy molecules and by cross‐talk between discrete pathways. The character and concentration of the available estrogen are determined by the extent of its biosynthesis, its penetration of the cell, and its subsequent metabolism. In addition, the estrogen affects its own access through stimulation of facilitating peptide hormones, prolactin, and sex hormone‐binding globulin. Finally, the induction of BPH is shown to be determined by the androgen/estrogen ratio and the change in stromal/epithelial balance accompanying aging. CONCLUSIONS Despite a growing knowledge of hormone levels, metabolism, and activities in the prostate, and the variety of processes and factors they affect, our explanation of BPH is still fanciful. Prostate 41:263–274, 1999. © 1999 Wiley‐Liss, Inc.

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“…(ii) Does the prostate accumulate ALA? We have found only three reports that discuss human prostate FA levels (13,23,24). Of these, only two have reported ALA levels in the prostate tissue, with values ranging from 0.5 to 2.7% of total FA (13,23).…”

mentioning

confidence: 99%

“…We have found only three reports that discuss human prostate FA levels (13,23,24). Of these, only two have reported ALA levels in the prostate tissue, with values ranging from 0.5 to 2.7% of total FA (13,23). One of these studies showed that the ALA levels in prostate tissue were significantly lower in the patients with advanced cases of prostate cancer than in the control subjects (13).…”

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confidence: 99%

α‐Linolenic acid and the risk of prostate cancer

Attar-Bashi

Sinclair

2004

Lipids

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Sir:Although the role of individual FA in cancer has been poorly investigated (1), a number of recent prospective epidemiological and case-control studies have shown a positive relationship between α-linolenic acid (ALA) in diet or blood and prostate cancer (2-8). In contrast, other epidemiological studies have found no significant relationship between ALA in diet, blood, or adipose tissue and prostate cancer (9-15). The

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Fatty acid composition of phospholipids in epithelium and stroma of human benign prostatic hyperplasia

Cited by 22 publications

References 30 publications

Phorbol ester stimulates ethanolamine release from the metastatic basal prostate cancer cell line PC3 but not from prostate epithelial cell lines LNCaP and P4E6

Phorbol ester stimulates ethanolamine release from the metastatic basal prostate cancer cell line PC3 but not from prostate epithelial cell lines LNCaP and P4E6

Estrogen in the etiopathogenesis of BPH

α‐Linolenic acid and the risk of prostate cancer

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