A search for a hormone-sensitive inositol lipid pool in WRK 1 mammary tumour cells

1989 ◽  
Vol 17 (1) ◽  
pp. 88-89 ◽  
Author(s):  
SARAH H. MACCALLUM ◽  
PHILIP A. HUNT ◽  
ROBERT H. MICHELL ◽  
CHRISTOPHER J. KIRK
Keyword(s):  
Tumour Cells ◽  
Mammary Tumour ◽  
Lipid Pool ◽  
Hormone Sensitive

scholarly journals Effect of dual agonists on phosphoinositide pools in WRK-1 cells

1990 ◽  
Vol 269 (3) ◽  
pp. 633-637 ◽  
Author(s):  
M E Monaco ◽  
M Attinasi ◽  
K Koréh
Keyword(s):  
Time Course ◽  
Inositol Phosphates ◽  
Subsequent Treatment ◽  
Tumour Cells ◽  
The Other ◽  
Mammary Tumour ◽  
Lipid Pool ◽  
Phosphoinositide Cycle ◽  
Heterologous Desensitization ◽  
Hormone Sensitive

Both vasopressin and bradykinin activate the phosphoinositide cycle in WRK-1 rat mammary tumour cells. When the two agonists are added simultaneously, partial additivity is observed with respect to disappearance of prelabelled phosphoinositides and accumulation of inositol phosphates; no additivity is observed with respect to resynthesis of phosphatidylinositol as assessed by monitoring [32P]Pi incorporation. Lack of complete additivity can be explained, at least in part, by heterologous desensitization. In order to determine whether the two agonists were accessing a common or individual hormone-sensitive phosphoinositide pools, cells were incubated with [32P]Pi in the presence of either vasopressin or bradykinin and subsequently restimulated with the alternative agonist. The lipid pool labelled in the presence of either agonist was sensitive to subsequent treatment by the other ligand, suggesting a common phosphoinositide pool. However, when cells were incubated with [32P]Pi in the absence of agonists, the time course of labelling of the hormone-sensitive pool was different for bradykinin and vasopressin, with that for bradykinin becoming labelled within a much shorter time. Thus although there is a significant overlap between the phosphoinositide pools responding to vasopressin and bradykinin, there is a small fraction of the hormone-sensitive lipid which responds only to bradykinin.

scholarly journals Isolated Flavonoids against Mammary Tumour Cells LM2

2009 ◽  
Vol 64 (1-2) ◽  
pp. 32-36 ◽  
Author(s):  
Camila B. de A. Carli ◽  
Djamile C. de Matos ◽  
Flávia C. M. Lopes ◽  
Danielle C. G. Maia ◽  
Maristela B. Dias ◽  
...  
Keyword(s):  
Antitumour Activity ◽  
Tumour Necrosis Factor Alpha ◽  
Tumour Cells ◽  
Mammary Tumour ◽  
Sandwich Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Almost All ◽  
Necrosis Factor

1The purpose of the present study was to investigate antitumour and anti-inflammatory activities of flavonoids isolated from Byrsonima crassa, Davilla elliptica and Mouriri pusa. The antitumour activity was measured by the MTT assay in murine mammary tumour cells (LM2) and the IC50 values of the fl avonoids tested ranged from (31.5 ± 2.97) to (203.1 ± 5.9) μg/ml. The fl avonoids (myricetin-3-O-α-L-rhamnopyranoside) and 3 (quercetin-3-Ogalactopyranoside) from D. elliptica were the most active ones against the tumour cells. The same samples were tested to determine the inhibition of the release of nitric oxide (NO) and of the tumour necrosis factor-alpha (TNF-α) in murine macrophages by the Griess and ELISA sandwich assay, respectively. Almost all the samples showed inhibitory activity to the release of NO but not of TNF-α. Of all substances tested, flavonoids 2 (quercetin) and 6 (myricetin) may show promising activity in the treatment of murine breast cancer by immunomodulatory and antiproliferative activities.

The use of cells doubly labelled with [14C]inositol and [3H]inositol to search for a hormone-sensitive inositol lipid pool with atypically rapid metabolic turnover

1989 ◽  
Vol 122 (1) ◽  
pp. 379-389 ◽  
Author(s):  
S. H. Maccallum ◽  
C. J. Barker ◽  
P. A. Hunt ◽  
N. S. Wong ◽  
C. J. Kirk ◽  
...  
Keyword(s):  
Cell Lines ◽  
Inositol Phosphates ◽  
Phosphatidyl Inositol ◽  
Receptor Activation ◽  
Inositol Monophosphatase ◽  
Lipid Pool ◽  
Inositol Lipids ◽  
Prostaglandin F ◽  
Hormone Sensitive ◽  
Stimulation Of

ABSTRACT Some, though not all, previous studies have suggested that the inositol lipid which is hydrolysed during transmembrane signalling in response to receptor activation might be drawn from a metabolically discrete and relatively small hormone-sensitive lipid pool that turns over more rapidly than the bulk of membrane inositol lipid. In order to seek evidence for the existence of this putative hormone-sensitive lipid pool, we have double-labelled cells by growing them for 3 days in a medium containing [14C]inositol and then supplying them with [3H]inositol for the final 2 h before stimulation. We anticipated that stimulation of these doubly labelled cells might provoke the formation, from the postulated hormone-sensitive pool, of small quantities of relatively 3H-enriched inositol phosphates, and that these could be harvested from cells (provided that the cytosolic inositol monophosphatase and inositol 1,4-bisphosphate/inositol 1,3,4-trisphosphate 1-phosphatase activities are first inhibited by Li+). Experiments of this type, using both vasopressin-stimulated WRK1 rat mammary tumour cells and 3T3 mouse fibroblasts stimulated by prostaglandin F2α, have largely failed to demonstrate the formation of relatively 3H-enriched inositol phosphates. There was a tendency for phosphatidyl-inositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate to have slightly higher 3H: 14C ratios than phosphatidylinositol, but the 3H: 14C ratios of the inositol phosphates formed in stimulated cells were not substantially greater than the 3H: 14C ratios of the inositol lipids. We therefore conclude, at least for the two cell lines that we studied, that hormone-stimulated inositol lipid hydrolysis can call, either directly or indirectly, upon the majority of the inositol lipid complement of the stimulated cell. Journal of Endocrinology (1989) 122, 379–389

Murine Mammary Tumour Cells In Vitro. Ii. Recruitment of Quiescent Cells

1984 ◽  
Vol 17 (1) ◽  
pp. 79-89
Author(s):  
C. Anne Wallen ◽  
R. Higashikubo ◽  
L. A. Dethlefsen
Keyword(s):  
Tumour Cells ◽  
Mammary Tumour ◽  
Quiescent Cells

scholarly journals Anti-proliferative effects of γ-tocotrienol are associated with suppression of c-Myc expression in mammary tumour cells

2015 ◽  
Vol 48 (4) ◽  
pp. 421-435 ◽  
Author(s):  
P. Parajuli ◽  
R. V. Tiwari ◽  
P. W. Sylvester
Keyword(s):  
Tumour Cells ◽  
Mammary Tumour

scholarly journals Phorbol ester inhibition of the hormone-stimulated phosphoinositide cycle in WRK-1 cells

1986 ◽  
Vol 236 (1) ◽  
pp. 171-175 ◽  
Author(s):  
M E Monaco ◽  
R A Mufson
Keyword(s):  
Binding Affinity ◽  
Phorbol Ester ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Tumour Cells ◽  
Mammary Tumour ◽  
Phosphate Accumulation ◽  
Phosphoinositide Cycle ◽  
Inositol Phosphate Accumulation

WRK-1 rat mammary tumour cells respond to vasopressin with increased accumulation of inositol phosphates as well as increased precursor incorporation into phosphatidylinositol. The phorbol ester, phorbol 13-myristate 12-acetate (PMA) inhibits by 80% both inositol phosphate accumulation and increased precursor incorporation. This inhibition is much less evident at early times (2 min) than at later times (25 min). The vasopressin-induced rise in cytosolic free Ca2+ is inhibited in a similar manner. Oleoylacetylglycerol is inactive with respect to inhibition of vasopressin-induced increases in incorporation of 32P into phosphoinositides. PMA has no effect on vasopressin binding at saturating concentrations of the hormone and does not affect the binding affinity.

Murine Mammary Tumour Cells In Vitro. I. the Development of A Quiescent State

1984 ◽  
Vol 17 (1) ◽  
pp. 65-77 ◽  
Author(s):  
C. Anne Wallen ◽  
R. Higashikubo ◽  
L. A. Dethlefsen
Keyword(s):  
Tumour Cells ◽  
Mammary Tumour ◽  
Quiescent State
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