Glucocorticoids Stabilize HER-2/neu Messenger RNA in Human Epithelial Ovarian Carcinoma Cells

Karlan, Beth Y.; Jones, J. A.; Slamon, Dennis J.; Lagasse, Leo D.

doi:10.1006/gyno.1994.1090

Cited by 38 publications

(19 citation statements)

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“…When activated, erbB2 is a potent receptor strongly involved in cancer biology [17] and frequently involved in cross-talk with other signalling pathways, including those of cytokines [18]. The present findings suggest that dexamethasone signalling affects erbB2 signalling in a similar manner to findings in ovarian carcinoma epithelial cells [19].…”

Section: Discussionsupporting

confidence: 67%

ErbB receptor regulation by dexamethasone in mouse type II epithelial cells

Dammann

Nassimi²,

Liu³

et al. 2006

Eur Respir J

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Glucocorticoids stimulate foetal surfactant synthesis. Therefore, they are used in impending pre-term birth. One mechanism of action on surfactant synthesis is through the induction of neuregulin (NRG) secretion by foetal lung fibroblasts. The direct effects on signalling pathways, and specifically on erbB receptors in foetal type II cell surfactant synthesis, are less well understood.The present authors studied the effect of known promoters of foetal surfactant synthesis (namely dexamethasone and mature (i.e. NRG-containing) fibroblast-conditioned medium (FCM)) on erbB receptor activation, protein content and dimerisation patterns in foetal mouse lung type II cells.Dexamethasone inhibited surfactant synthesis in immature type II cells at day (d)16 of gestation, while the mature FCM had stimulatory effects. Both treatments directly stimulated surfactant synthesis in more mature (d17) cells. At this gestational day, dexamethasone had only a small effect on phosphorylation, but it stimulated the protein levels of all four erbB receptors. Dexamethasone effects were distinct from those of mature FCM, which stimulated both protein content and phosphorylation of all erbB receptors and of the signalling intermediate phospholipase Cc. Dexamethasone modulated erbB receptor dimerisation patterns, such that erbB2 became the main dimerisation partner for erbB4.In conclusion, dexamethasone signalling involves erbB receptors in foetal type II cells, in a manner similar to, but distinct from, neuregulin-containing fibroblast-conditioned medium signalling.KEYWORDS: Dimerisation, epidermal growth factor, neuregulin, phospholipase Cc, surfactant synthesis A ntenatal surfactant production by foetal lung type II epithelial cells is crucial for the perinatal transition from the aquatic intrauterine environment to the gaseous atmosphere. Insufficient surfactant production, a condition present mainly in pre-term infants, leads to respiratory distress syndrome (RDS) [1]. Antenatal glucocorticoids decrease the incidence of RDS by ,50%, but they do not change the incidence of bronchopulmonary dysplasia (BPD), a chronic lung disease affecting surviving preterm infants. Most BPD infants had RDS [2,3]. The pre-natal administration of glucocorticoids has both stimulatory and inhibitory effects on the developing lung [4].Mesenchyme-epithelial interactions play an important role in foetal lung development by controlling the appropriate initiation of foetal surfactant production. This cell-cell communication process was described .25 yrs ago and is stimulated by glucocorticoids in the immature lung [5]. However, there remains a lack of information on the exact signalling pathways and factors involved in both the fibroblast-type II cell communication process and how it is stimulated by glucocorticoids. A better understanding of these mechanisms is crucial for developing therapeutic strategies that will promote the optimal maturation of the foetal surfactant system while avoiding the deleterious side effects of glucocorticoid treatment....

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Section: Discussionsupporting

confidence: 67%

ErbB receptor regulation by dexamethasone in mouse type II epithelial cells

Dammann

Nassimi²,

Liu³

et al. 2006

Eur Respir J

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“…Receptors for glucocorticoids are present in tumour cells of almost 90% of ovarian cancers, and these hormones inhibit ovarian cancer cell growth (Karlan et al, 1994). It is therefore of interest that three epithelial cancer cell lines (SKOV-3, BG-1 and PEO-4) exhibit a low basal level of 11bHSD-1 that is unresponsive to inflammatory stimulation, yet have gained a basal level of 11bHSD-2 mRNA that, in the case of the PEO-4 cell line, is cytokine responsive.…”

Section: Discussionmentioning

confidence: 99%

Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas

et al. 2005

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Ovulation is believed to contribute to the development of ovarian cancers that derive from the ovarian surface epithelium (OSE). The process of ovulation is synonymous with inflammation and inflammatory cytokines such as interleukin-1a (IL-1a) have recently been shown to induce both inflammatory and anti-inflammatory responses in human OSE (HOSE) cells. In this study we directly compared levels of IL-1a-induced gene expression by analysing the levels of 11b-hydroxysteroid dehydrogenase (11bHSD) types 1 (11bHSD-1) and 2 (11bHSD-2), cyclooxygenase-2 (COX-2), IL-1 receptor (IL-1R) and glucocorticoid receptor a (GRa) mRNA between normal HOSE cells and cell lines derived from poorly differentiated (SKOV-3, BG-1, PEO-4) and well-differentiated (PEO-14) ovarian adenocarcinoma. In HOSE cell cultures, and to a lesser extent PEO-14 cells, the basal mRNA levels of COX-2 and 11bHSD-1 were relatively high and further shown to be induced in response to IL-1a (for HOSE cells; 420-fold, Po0.05 and PEO-14 cells; 43fold, Po0.05). However, whereas HOSE cells expressed a low level of 11bHSD-2 mRNA that was only mildly responsive to IL-1a (1.3-fold, Po0.001), all cell lines exhibited a higher basal level of 11bHSD-2 mRNA that was in some cases further stimulated in PEO-4 cells (five-fold; Po0.05) or suppressed in SKOV-3 cells (two-fold; Po0.01) in response to IL-1a. All cells tested expressed IL-1R and, with the exception of BG-1, GRa. These results indicate that cell lines derived from ovarian cancers have lost the ability to respond normally to inflammatory cytokines such as IL-1a. The finding that normal OSE cells, in contrast to cell lines derived from patients with ovarian adenocarcinoma, abundantly express 11bHSD-1 mRNA but are essentially devoid of 11bHSD-2 mRNA supports the concept that the pattern of 11bHSD isoform gene expression is a defining feature of neoplastic cellular transformation, which might have particular relevance to the ovary.

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“…[33][34][35][36][37] All cell lines were obtained from the American Tissue Type Collection (ATTC) and cultured and maintained according to the supplier's recommendations. TOV-112D (Cat.…”

Section: Cell Lines and Sample Preparationmentioning

confidence: 99%

Detection of novel biomarkers for ovarian cancer with an optical nanotechnology detection system enabling label-free diagnostics

Kaja

2012

J. Biomed. Opt

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Abstract. Ovarian carcinoma has the highest lethality rate of gynecologic tumors, largely attributed to the late-stage diagnosis of the disease. Reliable tools for both accurate diagnosis and early detection of disease onset are lacking, and presently less than 20% of ovarian cancers are detected at an early stage. Protein biomarkers that allow the discrimination of early and late stages of ovarian serous carcinomas are urgently needed as they would enable monitoring pre-symptomatic aspects of the disease, disease progression, and the efficacy of intervention therapies. We compare the absolute and relative protein levels of six protein biomarkers for ovarian cancer in five different established ovarian cancer cell lines, utilizing both quantitative immunoblot analysis and a guided-mode resonance (GMR) bioassay detection system that utilizes a label-free optical biosensor readout. The GMR sensor approach provided highly accurate, consistent, and reproducible quantification of protein biomarkers as validated by quantitative immunoblotting, as well as enhanced sensitivity, and is therefore suitable for quantification and detection of novel biomarkers for ovarian cancer. We identified fibronectin, apolipoprotein A1, and TIMP3 as potential protein biomarkers for the differential diagnosis of primary versus metastatic ovarian carcinoma. Future studies are needed to confirm the suitability of protein biomarkers tested herein in patient samples.

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Glucocorticoids Stabilize HER-2/neu Messenger RNA in Human Epithelial Ovarian Carcinoma Cells

Cited by 38 publications

References 0 publications

ErbB receptor regulation by dexamethasone in mouse type II epithelial cells

ErbB receptor regulation by dexamethasone in mouse type II epithelial cells

Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas

Detection of novel biomarkers for ovarian cancer with an optical nanotechnology detection system enabling label-free diagnostics

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