Prostaglandin biosynthesis and stimulation of cyclic AMP in primary monolayer cultures of epithelial cells from mouse mammary gland

Gagnon, G.; Hunter, Sheila A.; Maudsley, David V.

doi:10.1016/0090-6980(76)90176-3

Cited by 18 publications

(3 citation statements)

References 22 publications

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“…Using chromatography and radioimmunoassay, we have obtained evidence that extracts of breast tumours contain prostaglandin E rather than prostaglandin F. Other studies using bioassay indicate that various prostaglandins may be present, and that 'prostaglandin F' may be predominant in extracts of some tumours (Bennett et al, , 1977. It is of interest in this context that some animal tumours and tumour cell lines produce predominantly, and sometimes exclusively, prostaglandin E2 (Tashjian et al, 1972;Hammarstrom, Samuelsson & Bjursell, 1973;Hamprecht, Jaffe & Philpott, 1973;Voelkel el al., 1975;Burstein, Gagnon, Hunter & Maudsley, 1976. Pros-M .…”

Section: Benign Breastmentioning

confidence: 97%

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

et al. 1980

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Amounts of prostaglandin E and prostaglandin F have been measured by radioimmunoassay in extracts of renal cortical carcinoma and benign and malignant breast tumours after solvent extraction and column chromatography. 2. Substantial amounts of prostaglandin E were found in extracts of benign and malignant breast tumours and in renal tumours. Much lower amounts of prostaglandin F were present in all tumour types. 3. Co-cultivation of tumour explants with mouse calvaria led to significant bone resorption in 10 of 13 renal carcinomas, three of eight malignant breast tumours, and two of nine benign breast tumours. Tumours associated with bone resorption had higher concentrations of prostaglandin E in culture media at the end of incubation than did non-resorbers. 4. Indomethacin (14 mumol/1) greatly reduced bone resorption in the presence of the tumour, but this was not always complete, particularly with breast tumours. Indomethacin had no effect on prostaglandin-induced bone resorption. Theophylline (2.2 mmol/1) significantly increased prostaglandin E production and resorption by an effect on the tumour. 5. It is concluded that prostaglandins may be important in mediating the effects of renal cortical carcinoma and possibly breast cancer on bone destruction. A non-prostaglandin mechanism may also contribute to bone destruction by breast carcinoma.

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Section: Benign Breastmentioning

confidence: 97%

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

et al. 1980

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“…Yet the exact mechanisms of action of PGF2a are not known. While a function via cAMP could be excluded (Sweat & Wincek 1973;Remold-O'Donnel 1974;Burstein et al 1976;Okamura & Terayama 1977), a stimulation of cGMP synthesis is still under discussion (Kuehl et al 1973).…”

mentioning

confidence: 97%

The effect of prostaglandins in the rat ovary: specific or unspecific stimulation of cAMP, cGMP and progesterone?

Schindler¹,

Müller²,

Siebers

1982

Acta Endocrinologica

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Ovarian membranes of the rat do not specifically bind prostaglandin E2 at any stage of development. Attachment of [3H]prostaglandin E2 in the presence of an excess of unlabelled prostaglandin E2 increased in a linear fashion and was not saturable. Prostaglandin E2 stimulated cAMP accumulation by ovarian cells of all developmental stages. This effect was not saturable. An effect of prostaglandin E2 on cGMP levels was not observed. At high concentrations of prostaglandin E2 an increase of ovarian progesterone synthesis was detected. In comparison hCG stimulated progesterone synthesis at much lower concentrations. PGF2\g=a\increased cellular and extracellular cAMP at 1000-fold higher concentrations than PGE2 and did not affect cGMP levels.

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“…We have recently shown that linoleic acid, by virtue of its metabolism to arachidonic acid and prostaglandin Ez, enhances the growth stimulatory effect of EGF on normal mouse mammary epithelial cells in primary cell culture (Bandyopadhyay et al, 1987). Since prostaglandin E2 is known to elevate the level of intracel-lular cAMP in mammary cells (Burstein et al, 1976), it was hypothesized that a CAMP-dependent pathway could be associated with the onset of cell proliferation. Previous observations showing that cholera toxin, an activator of adenylate cyclase, also stimulated the proliferation of mouse mammary epithelial cells in serum (Yang et al, 1980) and serum-free medium (Imagawa et al, 1982) containing EGF further supported this hypothesis.…”

mentioning

confidence: 99%

Growth stimulation by PGE₂ and EGF activates cyclic AMP‐dependent and ‐independent pathways in primary cultures of mouse mammary epithelial cells

Imagawa

Bandyopadhyay

Wallace

et al. 1988

Journal Cellular Physiology

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Mammary epithelial cells from virgin Balb/c mice were isolated by collagenase digestion and cultured within collagen gels in serum-free basal medium containing insulin (10 micrograms/ml). Previous work has shown that linoleate or its metabolite, prostaglandin E2 (PGE2), stimulate the growth of these cells only in the presence of a growth stimulant such as epidermal growth factor (EGF). Since PGE2 can stimulate cyclic AMP (cAMP) production, the role of cAMP in linoleate and EGF-stimulated growth was examined. The cAMP phosphodiesterase inhibitor, IBMX (0.1 mM), was found to augment growth when cells were cultured in the presence of both EGF and linoleate or PGE2, but not either factor alone. These results indicated that EGF does not stimulate proliferation via cyclic AMP mediated events but could synergize with cAMP events if cAMP levels were elevated by PGE2. When assayed in cells plated on top of collagen-coated culture dishes, cellular cyclic AMP levels were stimulated by PGE2, but only marginally by EGF. Although the stimulation of endogenous cAMP by PGE2 and IBMX was insufficient to stimulate growth in the absence of EGF, exogenous dibutyryl-cAMP (greater than 100 micrograms/ml) was able to do so showing that a sustained, and high level of cAMP (greater than 100 micrograms/ml) could stimulate growth in insulin-containing basal medium. EGF was capable of enhancing the cellular sensitivity to dibutyryl-cAMP but the converse was not observed. cAMP stimulation of growth was dependent upon a superphysiological concentration of insulin (10 micrograms/ml) or a physiological concentration of somatomedin-C. These results indicate that the proliferation of mouse mammary epithelial cells can be stimulated separately or in synergism by cAMP-dependent or -independent events.

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Prostaglandin biosynthesis and stimulation of cyclic AMP in primary monolayer cultures of epithelial cells from mouse mammary gland

Cited by 18 publications

References 22 publications

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

The effect of prostaglandins in the rat ovary: specific or unspecific stimulation of cAMP, cGMP and progesterone?

Growth stimulation by PGE₂ and EGF activates cyclic AMP‐dependent and ‐independent pathways in primary cultures of mouse mammary epithelial cells

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Prostaglandin biosynthesis and stimulation of cyclic AMP in primary monolayer cultures of epithelial cells from mouse mammary gland

Cited by 18 publications

References 22 publications

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

Prostaglandins as Mediators of Bone Resorption in Renal and Breast Tumours

The effect of prostaglandins in the rat ovary: specific or unspecific stimulation of cAMP, cGMP and progesterone?

Growth stimulation by PGE2 and EGF activates cyclic AMP‐dependent and ‐independent pathways in primary cultures of mouse mammary epithelial cells

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Growth stimulation by PGE₂ and EGF activates cyclic AMP‐dependent and ‐independent pathways in primary cultures of mouse mammary epithelial cells