A common sequence of calcium and pH signals in the mitogenic stimulation of eukaryotic cells

Hesketh, T R; Moore, John P.; Morris, Jeremy; Taylor, Martin J.; Rogers, J. H.; Smith, Gavin; Metcalfe, James C.

doi:10.1038/313481a0

Cited by 448 publications

(165 citation statements)

References 35 publications

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“…alkalinization of the cytosol through proton extrusion via the Na+/H+ antiport [84], increase in cytosolic free calcium concentration [84], changes in intracellular NAD+/NADH ratio [85] and activation of 'immediate early genes' (e.g. c-myc and c-fos) [86] -may be triggered by stimulation of the NADH:ferricyanide oxidoreductase [40,41,[87][88][89][90].…”

Section: Transferrin and The Regulation Of Cell Growthmentioning

confidence: 99%

The role of transferrin in the mechanism of cellular iron uptake

Thorstensen

Romslo

1990

Biochemical Journal

185

105

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INTRODUCTIONThe role of transferrin and its cell surface receptor in cellular iron metabolism has received considerable interest during the last decade. Hence, over this period several reviews covering various aspects of the topic have been published.In this review we attempt to summarize the new knowledge and controversies encountered during the last 4-5 years. The focus is on iron metabolism by the hepatocyte. We also view the concept of transferrin-cell interactions from angles which previously may not have been given particular attention, and we include some aspects of iron metabolism not normally covered by reviews of this type. Central parts of what may be regarded as well-established knowledge either have been entirely omitted, or are only briefly described or mentioned to the extent considered relevant to the particular topic discussed. Important aspects of iron metabolism such as iron adsorption, haemochromatosis, ferritin iron and iron in infection and neoplasia are not covered in the present paper. Instead, the reader is referred to one or more of the recently published reviews [1-5] and references therein.

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Section: Transferrin and The Regulation Of Cell Growthmentioning

confidence: 99%

The role of transferrin in the mechanism of cellular iron uptake

Thorstensen

Romslo

1990

Biochemical Journal

185

105

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“…Intracellular content of Na+ and K+ is mainly regulated by the Na+/K+ ATPase, and in some cases the Na+/H+, antiport in cell membranes, whose activities have been shown to be activated by phorbol ester tumor promoters and growth factors such as platelet-derived growth factor [6,22,37,38,44,56,60]. There is evidence that Na+/K+ ATPase activation is linked to the enhancement of cell growth and of TPA-mediated transformation in C3HIOT1/2 cells, and that a tumor promotion inhibitor, retinoic acid, inhibits TPA-mediated activation of the Na+/K+ ATPase in C3H10T1/2 [3].…”

Section: Regulation Of Cell Communication and Cell Growthmentioning

confidence: 99%

Modulation of cell communication and carcinogenesis.

Kanno

1985

Jpn.J.Physiol

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In many types of tissue and culture cells, the interiors of adjacent cells communicate with each other through cell-to-cell channels. The fine structure of the cell-to-cell channel has been well studied and defined as a gap junction which consists of six identical, rod-shaped protein subunits [59]. This transmembrane channel permits free exchange of ions and small molecules between contacting cells [53]. This type of interaction between cells has been called "gap junctionalThis communication is readily proved by three different methods : electrophysiological, fluorescent dye transfer and metabolic cooperation methods [33].Cell communication has been thought to be regulated by the concentration of intracellular Ca2+ [45,46] and CAMP [17]. Calcium ion produces graded changes in cell communication [47]. cAMP modulates cell communication by stimulating the de novo synthesis of gap junctional protein [17].Since extensive reviews on the general properties of the gap junction and its physiological role have appeared in recent years [33,34], this short review will deal with a limited topic, namely, recent studies on the physiological role of gap junctional cell communication in the phenotypic manifestation of cancer. I. CELL COMMUNICATION IN CANCER CELLSInvestigation of cell communication in cancer cells was first made in rat liver tumors including primary, Morris and Novikoff hepatomas by electrophysiological methods [35]. Subsequently, similar studies were performed in transplanted rat and hamster thyroid tumors [24] and human stomach carcinoma [28]. These earlier studies showed a lack or a decrease of cell communication between contacting cancer cells, indicating the predominance of communication-incompetent cells in malignant tumors. A solid tumor, which was developed by transplantation of MH 134 cells into the subcutaneous space of C3H/He mice showed a decreased level of communication as revealed by electrical coupling. The decrease of cell communication appeared to correlate with the characteristics of metastasis in the case of MH 134 cells [23]. In benign tumors, such as human follicular adenoma, human diffuse toxic goiter and nontoxic nodular goiter, con-

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“…The PIP2-hydrolysing agonists induce an 1P3-mediated mobilization of intracellular Ca2+ from bound stores, which can be demonstrated either as an increased efflux of 45Ca2+ from pre-labelled cells Lopez-Rivas & Rozengurt, 1984) or as an elevation of intracellular free Ca2+ concentration measured with quin2 (Hesketh et al, 1985;Mendoza et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Protein kinase C-mediated negative-feedback inhibition of unstimulated and bombesin-stimulated polyphosphoinositide hydrolysis in Swiss-mouse 3T3 cells

Brown

Blakeley

Hamon

et al. 1987

Biochemical Journal

113

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Bombesin-related peptides stimulate a rapid increase in polyphosphoinositide hydrolysis in Swiss-mouse 3T3 cells. These peptides generate an increase in the efflux of 45Ca2+ from pre-labelled cells, a response consistent with an inositol trisphosphate-mediated mobilization of intracellular Ca2+. The bombesin-stimulated release of cellular 45Ca2+ is inhibited by tumour-promoting phorbol esters (e.g. 12-0-tetradecanoylphorbol 13-acetate, TPA). Although there are several possible sites of action at which this effect might occur, our results indicate that TPA induces an uncoupling of bombesin-stimulated hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) without decreasing cellular binding of bombesin. In cultured cells, protein kinase C can be down-modulated by a prolonged incubation of the cells with phorbol esters. Such pretreatment greatly decreased the inhibitory effect of TPA on bombesin-stimulated PIP2 hydrolysis, suggesting that this action of the phorbol ester is mediated via protein kinase C. Since diacylglycerol is an endogenous activator of protein kinase C and a direct product of PIP2 hydrolysis, these results suggest that protein kinase C inhibition of polyphosphoinositide hydrolysis may function as a negative-feedback pathway. Cells in which protein kinase C has been down-modulated show elevated basal and bombesin-stimulated production of inositol phosphates, providing evidence that such a feedback loop limits polyphosphoinositide turnover in both unstimulated and mitogen-stimulated cells.

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A common sequence of calcium and pH signals in the mitogenic stimulation of eukaryotic cells

Cited by 448 publications

References 35 publications

The role of transferrin in the mechanism of cellular iron uptake

The role of transferrin in the mechanism of cellular iron uptake

Modulation of cell communication and carcinogenesis.

Protein kinase C-mediated negative-feedback inhibition of unstimulated and bombesin-stimulated polyphosphoinositide hydrolysis in Swiss-mouse 3T3 cells

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