Density-dependent tumor cell death and reversible cell cycle arrest: Mutually exclusive modes of monocyte-mediated growth control

Bosch, Jürgen; Rüller, Stephan; Horn, Dániel; Schumann, Ralf R.; Schlaak, M

doi:10.1016/0014-4827(90)90080-t

Cited by 20 publications

(30 citation statements)

References 41 publications

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“…While for the moment we are unaware of the signif icance of this finding, it could be related to an increase in survival of cells in Go/Gi. Indeed, there is evidence that Go/Gt cells can escape immune attack [33][34][35][36] and it is known that cells enter Go under inadequate conditions [37,38], The progression of cells through the cell cycle is associ ated with an orderly series of events, some of which con trol the expression of cell surface macromolecules. The la molecule has been reported to be associated with a certain phase cycle [39].…”

Section: Discussionmentioning

confidence: 99%

Enhancement of la Antigen Expression and Nonproliferating Cells Correlates with Metastatic Capacity

et al. 1994

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Maintaining B16F10 tumor cells in stirring culture for 48 h leads to an increase in lung and liver colonizing capacity in comparison with cells in adherent culture. Parallel to the increased metastatic capacity, we have observed a decrease in the proliferative rate of tumor cells (as the percentage of proliferating cell nuclear antigen-positive cells) and an increase in the population of tumor cells expressing la antigen. These results are not exclusive to B16F10 cells, since the same results were obtained when we analyzed 3LL cells maintained in identical culture conditions. In all the tumor lines tested, we found an association between the nonproliferating and the la-positive cell populations. We induced la expression by treating B16F10 cells in adherent culture with the lectin concanavalin A and again, coincident with an increase in metastatic capacity, we found the same association between the two parameters analyzed – nonproliferating state and la antigen expression. In addition, it was found that B16F10 cells induce lymphocytic proliferation, and a direct relationship was established between the number of Ia+ cells and lymphocytic proliferation.

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Section: Discussionmentioning

confidence: 99%

Enhancement of la Antigen Expression and Nonproliferating Cells Correlates with Metastatic Capacity

et al. 1994

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“…SU gained from MOiTC inter-action cultures closely mimic the effects exerted by MO on TC during direct interaction (Van der Bosch et al, 1990;Horn et al, 1991). The following characteristics are especially to be mentioned.…”

Section: A : @----*)mentioning

confidence: 96%

“…l a : *----*I. It has been demonstrated previously by flow cytometric cell cycle analysis that exposure to MO or SU leads t o accumulation of the entire TC population in G1 within 16 to 24 h ( Van der Bosch et al, 1990;Horn et al, 1991). In the present work cell cycle phase distributions were determined routinely by recording nuclear size distributions, which have been shown to reflect closely cellular DNA content (Butler, 1984).…”

Section: A : @----*)mentioning

confidence: 98%

“…It consists of a 1 + 1 mixture of DMEM + Ham's F12 buffered by 22 mM NaHCO, and 15 mM HEPES (DF) and is supplemented by insulin (5 pgiml), transferrin (5 pgi ml), epidermal growth factor (EGF) (5 nglml), triiodothyronine (0.1 nM), Na-selenite (75 nM), ethanolamine (8 pM), oleic acid (2.5 pgiml), and fatty acid-free albumine (0.6 mgiml). Establishment of the clonal human tumor cell lines A375-1, A375-2, and A375-7 from the A375 melanoma cell line, and of BT-A, BT-B, BT-C, and BT-D from a surgical specimen of a bladder carcinoma have been also described previously (Van der Bosch et al, (1990). For passaging, cultures were washed twice with 10 ml of 0.9% NaCli 10 nM HEPES, pH 7.4 (NaClI HEPES) and detached with 20 pg trypsin per ml NaCli HEPES.…”

Section: Cell Culturementioning

confidence: 99%

“…Within 10 min under this condition, TC membranes are lysed quantitatively, whereas TC nuclei are swollen and released as intact entities, which after 2 h of fixation with 0.5 ml 10% formaldehyde and transfer into 2 ml of 1.8% NaCl can be counted electronically as described previously (Van der Bosch et al, 1990).…”

Section: Cell Culturementioning

confidence: 99%

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Modulation of tumor cell susceptibility to cytokine‐induced cell death by hormones, growth factors, and cell density

Bosch¹,

Horn²,

Rüller³

et al. 1992

Journal Cellular Physiology

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The mechanisms controlling "spontaneous" cellular death rates in normal and tumorigenic tissues are largely unknown. An important parameter in this respect is the susceptibility of the target cell to induction of the lytic pathway by appropriate signals. In the present article it is demonstrated in a serum-free in vitro system that the susceptibility of human tumor cells (TC) to induction of lysis by cytokine signals generated during interaction of TC with elutriated human monocytes (MO) is a highly dynamic parameter subject to modulation by hormones, growth factors, and tumor cell density. It was found that growth stimulatory signals such as insulin, and especially epidermal growth factor (EGF), increase lytic susceptibility, whereas hydrocortisone, which does not exert significant growth modulatory effects in these examples, protects TC against the induction of lysis. Increasing TC density above confluence dramatically enhances lytic susceptibility, suggesting interactions between TC to be involved in the induction of their death. In conjunction with previous data demonstrating the insusceptibility of TC, which are forced out of the cell cycle into the quiescent state (G0), the hypothesis is put forward that growth stimulatory factors increase a TC's lytic susceptibility by preventing its transit from G1 to G0 in response to growth inhibitory signals generated during MO/TC interaction. The data support the concept that TC susceptibility to the induction of cell death is a consequence of simultaneously activated growth stimulatory and growth inhibitory signalling pathways.

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Suppression of tumor cell susceptibility to monocyte‐induced cell death by growth‐inhibitory signals generated during monocyte/tumor cell interaction

Horn

Bosch

Rüller

et al. 1991

J of Cellular Biochemistry

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In a recently established serum-free in vitro system it has been demonstrated that the susceptibility of various human tumor cells to the induction of cell death by elutriated human monocytes is critically dependent on tumor cell density and growth state. In the present work it is shown by flow cytofluorometric analysis of bromodeoxyuridine incorporation rates and of expression of the proliferation-associated nuclear antigen Ki-67, that tumor cells forced out of the cell cycle into the quiescent state (G0), which can be accomplished by treatment with supernatant from monocyte/tumor cell interaction cultures, are no longer susceptible to the induction of cell death by monocytes. This suggests that processes essential for the lytic pathway cannot take place in quiescent cells. It is furthermore demonstrated that tumor cells are driven into G0 during interaction with monocytes and that the rate of transit from G1 to G0 increases with increasing monocyte dosage. This explains our earlier finding that maximum rates of tumor cell death are induced at rather low monocyte:tumor cell ratios of around 1:2 and that lysis is suppressed at higher monocyte dosages (van der Bosch et al.:Exp Cell Res 187:185-192, 1990). The potential significance of these findings for the supposed function of mononuclear phagocytes in tumor defense lies in the notion that tumor cells driven into G0 might escape this control and that signals involved in monocyte/tumor cell-interaction contribute to the accumulation of tumor cells in G0.

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Density-dependent tumor cell death and reversible cell cycle arrest: Mutually exclusive modes of monocyte-mediated growth control

Cited by 20 publications

References 41 publications

Enhancement of la Antigen Expression and Nonproliferating Cells Correlates with Metastatic Capacity

Enhancement of la Antigen Expression and Nonproliferating Cells Correlates with Metastatic Capacity

Modulation of tumor cell susceptibility to cytokine‐induced cell death by hormones, growth factors, and cell density

Suppression of tumor cell susceptibility to monocyte‐induced cell death by growth‐inhibitory signals generated during monocyte/tumor cell interaction

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