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Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
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Human lung cancers overexpress several cell-membrane complement inhibitory proteins (CIP). These
complement inhibitory proteins are membrane cofactor protein (CD46), decay-accelerating factor (DAF;
CD55), and CD59 (protectin). These cell-membrane proteins have a wide normal tissue distribution, are
known to protect normal host cells from homologous complement-mediated lysis, and are thought to facilitate tumor escape from immunosurveillance. To study whether proinflammatory cytokines that are involved in cancer growth can modulate cell-membrane CIP expression in lung cancer cells, we studied the
effect of interleukin (IL)-1
, tumor necrosis factor (TNF)-, and interferon (IFN)-
on two human lung
cancer cell lines. ChaGo K-1 and NCI-H596 cell lines, undifferentiated carcinoma and lung adenosquamous carcinoma, respectively, were stimulated with different cytokines, and the effects of incubation time
and cytokine concentration on cell-membrane CIP expression were studied. Cell-membrane CIP expression was evaluated using flow cytometry and cytokine effect was calculated as percent change in mean
fluorescence intensity of each CIP molecule from its untreated control. We found that DAF was the lung
cancer cell-membrane CIP molecule that was the most responsive to cytokine stimulation. Maximal stimulatory effect was usually noted 72 h after a cytokine was introduced. In ChaGo K-1 and NCI-H596 lung
cancer cell lines, IL-1 and TNF- increased DAF expression. IL-1 (100 U/ml/72 h) increased DAF expression up to a maximal mean of 45 and 48%, respectively, in comparison with untreated cells. TNF-
(1,000 U/ml/72 h) increased DAF expression up to a mean of 131 and 46%, respectively. IFN- (1 U/ml/72
h) increased DAF expression in NCI-H596 cells up to a mean of 100%, but had a slight inhibitory effect on
DAF expression in ChaGo K-1 cells, decreasing expression by a mean of 17% in comparison with untreated cells. We conclude that cell-membrane DAF expression in the studied human lung cancer cell lines is modulated by IL-1, TNF-, and IFN-, and speculate that cytokine-mediated modulation of cell-membrane
DAF in human lung cancer cells might affect lung cancer cell biology.
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Introduction |
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Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
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Membrane cofactor protein (MCP; CD46) (1), decay- accelerating factor (DAF; CD55) (2), and CD59 (3), are cell-membrane complement inhibitory proteins (CIP). These proteins are aimed to protect human cells from lysis by homologous complement and have a wide tissue distribution. The human respiratory tract, although frequently exposed to complement and to complement activators (4), has been poorly investigated with regard to possible interrelationships existing between respiratory epithelium and the complement system. Recently, we described the expression and distribution of CD46, CD55, and CD59 along the
human respiratory tract in health and in disease, including lung cancer (8), and demonstrated their functional role in protecting normal human respiratory epithelium from complement-mediated lysis in vitro (9).
Human lung cancer arises from bronchial respiratory epithelium, is unresponsive to immunotherapy, and is considered the most lethal human cancer. If lung cancer cells, being foreign cells, could be specifically lysed by complement using immunotherapy with tumor-associated monoclonal antibodies (mAb), lung cancer growth and metastasis would be hampered. However, one of our recent in vivo observations was that human lung cancer expresses higher levels of cell-membrane CIP in comparison with normal respiratory epithelium (8). We confirmed this observation in a more quantitative way in vitro using human lung cancer cell lines that showed constitutive differences in CIP expression. These lung cancer cell lines were also found to exhibit extreme resistance to complement-mediated lysis (10).
Increased in vivo expression of protective cell-membrane CIP molecules in human lung cancer might result
not only from a constitutive mechanism but also from microenvironmental influences. Microenvironmental influences on lung cancer CIP expression, to our knowledge,
have not been investigated so far. In the present study we
investigated whether the cytokines interleukin (IL)-1,
tumor necrosis factor (TNF)-, and interferon (IFN)-,
which can be generated at cancer microenvironment and
may affect cancer growth and metastasis (11), can
modulate expression of cell-membrane CIP in human lung
cancer in vitro. In addition, we investigated whether dexamethazone (Dex), an agent that usually modulates the effects of many proinflammatory cytokines, can also do so in
this in vitro system.
For these purposes we studied two human non-small-cell lung cancer cell lines, NCI-H596 and ChaGo K-1, that
we studied previously for aspects of cell-membrane CIP
(10). We assessed cell-membrane expression of CD46,
CD55, and CD59 by flow cytometry in cancer cells that
were or were not stimulated by IL-1, TNF-, and IFN-. In some experiments we tested the influence of Dex treatment on the modulatory effect of the cytokine that was
found to be the most potent.
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Materials and Methods |
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Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
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Human Lung Cancer Cells
Two human non-small-cell lung cancer cell lines were obtained from the American Type Culture Collection (ATCC; Rockville, MD). Cell lines were ChaGo K-1 (undifferentiated bronchogenic carcinoma, ATCC No. HTB 168) and NCI-H596 (adenosquamous bronchogenic carcinoma, ATCC No. HTB 178). Cells were seeded and grown to confluency in uncoated 25-cm2 plastic culture flasks. Culture medium was changed at 3-d intervals and consisted of 90% RPMI-1640 (Biological Industries, Beit-Haemek, Israel), 10% fetal bovine serum (GIBCO BRL Life Technologies, Paisley, Scotland), and antibiotics (penicillin, 100 U/ml; streptomycin, 100 µg/ml).
Cytokines and Antibodies
Cytokines were added to the human lung cancer cell cultures 96 h after cell seeding. Human rIL-1 (1 µg = 1.6 × 105 U), human rTNF- (1 µg = 1.1 × 105 U), and human
rIFN- (1 µg = 104 U) were all purchased from R&D Systems (Minneapolis, MN).
Monoclonal antibodies were used to assess expression of the specific cell-membrane CIP molecules by flow cytometry. Mouse antihuman MCP mAb J4-48 (immunoglobin G1 [IgG1], 1 mg/ml) (16), mouse antihuman DAF mAb BRIC 216 (IgG1, 1 mg/ml) (17), and rat antihuman CD59 mAb YTH 53.1 (IgG2b, 0.5 mg/ml) (3) were all purchased from Serotec (Oxford, UK).
Fluorescein isothiocyanate (FITC)-conjugated secondary F(ab')2 antibodies for flow cytometry studies were purchased from Jackson Immunoresearch Lab (West Grove, PA)
Cytokine Stimulation Protocols
Each cytokine, dissolved in a fresh culture medium, was added to a cell-line culture flask 96 h after cells were seeded. In one set of experiments, cytokine time-dependent effects on cell-membrane expression of CIP were evaluated by incubating cell cultures with a fixed concentration of a specific cytokine for 24, 48, and 72 h without changing the medium thereafter. Control experiments were done identically by adding culture medium without the cytokine. In another set of experiments, cytokine concentration-dependent effects were evaluated by adding a specific cytokine at different concentrations for a fixed time of 72 h.
When cytokine stimulation experiments were ended, the culture medium was aspirated and cell cultures were prepared for flow cytometry analysis of cell-membrane CIP.
Dex Effect
In some experiments we tested the ability of Dex to influence the modulatory effect of a specific cytokine on a specific cell-membrane CIP. Cell cultures, 72 h after cell seeding, were incubated with fresh medium containing Dex
10
7 or 106 M for 96 h. Twenty-four hours after Dex was
introduced, TNF- (1,000 U/ml) and IFN- (100 U/ml)
were added for 72 h to the Dex-containing media of
ChaGo K-1 and NCI-H596 cell lines, respectively. In control experiments, some cell cultures were treated the same
with TNF- or IFN- but Dex was omitted, and other cell
cultures were treated by medium alone and by medium
plus Dex. At the end of the incubation time cells were prepared for flow cytometry analysis.
Flow Cytometry Analysis of Cell-membrane CIP
Expression of MCP, DAF, and CD59 in ChaGo K-1 and NCI-H596 human lung cancer cell lines that were or were not stimulated by cytokines was assayed by flow cytometric analysis. Cancer cell cultures in flasks were first rinsed with 2 ml of 0.25% trypsin-ethylenediamenetetraacetic acid (EDTA) solution that was immediately aspirated; flasks were then placed in a cell culture incubator for 5 to 7 min. Cells were then aspirated, mechanically dispersed with a pipette, and extensively washed by phosphate-buffered saline (PBS) containing 10% heat-inactivated fetal calf serum.
Cell viability by trypan blue was always greater than 96% for all cell types treated by trypsin-EDTA. Cells were resuspended in "enriched" PBS (containing Ca+2, Mg+2 [1 mM each], bovine serum albumin, and glucose [0.5% each]), and were incubated with primary antibodies for the various cell-membrane CIP (30 min, 4°C) with gentle shaking. Cells were then washed twice in "enriched" PBS, and incubated with appropriate secondary antibodies, goat F(ab')2 antirat IgG or goat F(ab')2 antimouse IgG, both FITC-conjugated (30 min, 4°C). Cells were then extensively washed and resuspended in ice-cold PBS (0.5 ml) at a cell concentration of 106/ml and analyzed by a flow cytometer (Epics Profile II Flow Cytometer; Coulter Electronics, Luton, UK). The flow cytometer was equipped with an argon ion laser, using 15 MW light with an excitation wavelength of 488 nm and detection wavelength of 525 nm. The voltage used was 850 V. A total of 5,000 cells were analyzed by gating on a uniform cell population on a two-parameter histogram of forward-versus-side scatter. The fluorescence histograms were overlaid to determine significant differences from negative control antibodies. For negative control we used the appropriate FITC-conjugated secondary antibodies, or FITC-conjugated goat serum antihuman IgD (Kallestad Laboratories, Chaska, MN).
In preliminary studies we first determined the optimal dilution of primary antibodies needed to saturate each type of cell-membrane CIP on each cancer cell line. We used these optimal dilutions for our further assays. The effect of cytokine or Dex treatment on expression of CIP molecules was expressed as percent change of the mean fluorescence intensity (MFI) from its untreated control cells, as follows:
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(1) |
Data Analysis
Mean values of the various treatment groups were compared with a one-way analysis of variance (ANOVA).
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Results |
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Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
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DAF (CD55) in both human lung cancer cell lines was the cell-membrane CIP that was the most responsive to cytokine stimulation.
Cytokine Time-dependent Effects
In time-effect experiments the various cytokines had a more pronounced modulatory effect on CIP expression after 48 to 72 h of incubation with either lung cancer cell line (Figure 1).
|
IL-1 and TNF-, when used alone, had consistent
time-dependent upregulatory effects on DAF expression
in both lung cancer cell lines (Figure 1). TNF- was more
effective in ChaGo K-1 cells than in NCI-H596 cells. IL-1
and TNF-, when used alone, had no effect on expression
of MCP and CD59 in either cell line (data not shown).
When IL-1 and TNF- were used in combination, their
time-dependent upregulatory effect on DAF expression in
both cell lines was additive (Figure 1). A combination of
IL-1 and TNF- also had a slight upregulatory time-dependent effect on expression of MCP in ChaGo K-1 cells and
on CD59 of NCI-H596 cells (Figure 2).
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IFN- had a marked time-dependent upregulatory effect on DAF expression, but only in NCI-H596 cells. IFN-
upregulatory effect was more pronounced than the effect
of IL-1 or TNF- on DAF expression in these cells (Figure 1).
In ChaGo K-1 cells, IFN- had a slight downregulatory
effect on DAF expression, decreasing expression to a
mean of 17% below expression in untreated cells (Figure
1). IFN- had no effect on expression of MCP and CD59
in either lung cancer cell line (data not shown).
Cytokine Concentration-dependent Effects
In both human lung cancer lines the cytokine concentration-dependent effects on DAF expression were studied after 72 h of cell stimulation. We chose to study DAF expression because in time-dependent experiments DAF was found to be the most responsive protein.
In the ChaGo K-1 cell line, IL-1
and more so TNF-
upregulated DAF expression in a concentration-dependent way. IL-1 (100 U/ml/72 h) and TNF- (1,000 U/ml/
72 h) increased DAF expression up to a mean of 45 and
131% change in MFI, respectively (Figure 3).
|
Similarly, in NCI-H596 lung cancer line, IL-1 and
TNF- upregulated DAF expression in a concentration-dependent way, as they did in ChaGo K-1 cell lines, although
TNF- was more effective in ChaGo K-1 cells (Figure 4).
The effect of IFN- on DAF expression was also upregulatory and was the most pronounced. IFN- at 0.1 U/ml/72 h
increased DAF expression by 100%, and 1,000 U/ml had a
maximal increase of 140% over unstimulated cells as judged
from percent change in MFI (Figure 4).
|
Effect of Dex
Dex pretreatment of both lung cancer cell lines significantly inhibited the upregulatory effect of TNF- and
IFN- on DAF expression.
DAF expression in ChaGo K-1 cells in the presence of
TNF- alone and in the presence of both TNF- and Dex
was 139 and 33% above expression of DAF in untreated
cells, respectively (Figure 5). DAF expression in NCI-H596
cells in the presence of IFN- alone and in the presence of
both IFN- and Dex was 80 and 46% above expression of
DAF in untreated cells, respectively (Figure 5).
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Discussion |
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Abstract
Introduction
Materials and Methods
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Discussion
Conclusions
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This study demonstrates that IL-1, TNF-, and IFN-
can modulate cell-membrane expression of CIP in human
lung cancer cells in vitro. We showed that expression of
MCP, DAF, and CD59 is modulated to a variable extent
depending on the specific CIP molecule, the specific cytokine, and the type of lung cancer cell line.
Of all three lung cancer cell-membrane CIP molecules
that we studied, DAF was the one that was most responsive to cytokine stimulation. Maximal response occurred at
48 to 72 h after a cytokine was introduced. In both human
lung cancer cell lines, IL-1 and TNF- upregulated DAF
expression and their combination had a positive additive
effect. TNF- was especially potent in ChaGo K-1 undifferentiated lung cancer cells. Interestingly, IFN- had an
opposite regulatory effect on DAF expression in the two
different cell lines. IFN- was the most potent cytokine
with regard to upregulation of DAF expression in NCI-H596 adenosquamous lung cancer cells, but in ChaGo K-1
cells it had a moderate downregulatory effect on DAF expression. The reason for this difference in IFN- effect is unclear. Possibly it reflects the differences in lung cancer
cell type and in degree of cell differentiation of the tested
lines.
Regarding the marked responsiveness of DAF expression in human lung cancer cells, as we showed, it is worthwhile to note that DAF expression in tissues other than the
lung was also found by others to be especially responsive
to cytokines (18), suggesting that DAF may act as an
activation antigen. Our finding that Dex had an inhibitory
effect on TNF- and on IFN--mediated upregulation of
DAF expression in ChaGo K-1 and NCI-H596 cells, respectively, suggests that transcription factors are involved in
modulation of DAF expression by TNF- and IFN- (22).
In contrast to the marked responsiveness of DAF expression to cytokine stimulation of both lung cancer cell
lines, MCP expression was only slightly upregulated by a
combination of IL-1 and TNF- in ChaGo K-1 cells and
was not influenced by any cytokine in NCI-H596 cells.
CD59 expression was moderately upregulated by the combined effects of IL-1 and TNF- and only in NCI-H596
adenocarcinoma cells. A similar response of CD59 to IL-1
and TNF- in combination has been described in human
colonic adenocarcinoma cell line (19). The reason for the
marked difference between the responsiveness of DAF and
the responsiveness of MCP and CD59 to cytokine stimulation is not clear.
Expression of MCP, DAF, and CD59 in human lung cancer, in contrast to other cancers (23), was scarcely investigated (26, 27). Its biologic function in lung cancer has never been studied, to our knowledge. We recently described, semiquantitatively, an increased expression of these molecules in human lung cancer in vivo (8). We also demonstrated in a more quantitative way, using flow cytometry in the same two human lung cancer cell lines, an increased constitutive expression of these molecules in comparison with noncancer human respiratory epithelial cells under basal cell culture conditions (10 and unpublished data). The observed increase in CIP expression was accompanied by an increase in cell resistance to complement-mediated lysis.
Increased expression of lung cancer cell-membrane CIP
molecules in vivo theoretically may result from an increased constitutive expression but may also result from
effects of microenvironmental cytokines. IL-1, TNF-,
and IFN- are proinflammatory cytokines that are also
produced at cancer microenvironment and might affect cancer growth and metastasis (11). The effects of these
and other cytokines on cell-membrane expression of CIP
molecules of malignant and normal human cells were studied only recently and only in nonpulmonary cells (18).
The accumulating evidence supports our own findings in
lung cancer cells. It suggests that in normal and malignant
cells a specific cell-membrane CIP molecule, depending on
its tissue origin, may respond variably to a specific cytokine, and that different CIP molecules of a specific tissue
origin may respond variably to a specific cytokine. These
findings may explain in part the heterogeneity of cell-membrane CIP expression, which is also evident in various
carcinomas in vivo (27).
Cytokine-mediated regulation of DAF and CD59 expression may affect lung cancer cell biology. We have shown recently that phosphatidylinositol-specific phospholipase C-mediated detachment of cell-membrane DAF and CD59 from the same two human lung cancer cell lines results in extensive complement-mediated lysis of cells that were otherwise extremely resistant to complement (10). DAF and CD59 were also shown by others to protect cancer cells from complement-mediated lysis (2, 19, 23, 25, 28), and DAF was shown to impair NK cell activity against tumor cells (29). DAF may also participate in yet unknown cellular functions by intracellular signaling via tyroxine kinase of the src protein family (30).
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Conclusions |
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Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
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We conclude that IL-1, TNF-, and IFN-, proinflammatory cytokines that are also known to be produced at cancer microenvironment, can modulate expression of cell-membrane CIP in human lung cancer cells. DAF is the
most responsive protein in vitro. In vivo, cell-membrane CIP expression in lung cancer cells might be affected by
many more microenvironmental factors, such as other cytokines and growth factors. These microenvironmental
factors may upregulate or downregulate CIP expression.
The net result of cell-membrane CIP expression probably
depends on the balance achieved between these factors and the cancer cells in a specific host microenvironment.
Expression of lung cancer cell-membrane CIP molecules
and its modulation by tumor microenvironmental factors
may contribute to lung cancer escape from immunosurveillance, affect lung cancer growth and metastasis, or interfere with immunotherapy using tumor-associated mAb,
and should therefore be a target for further research.
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Footnotes |
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Address correspondence to: Shabtai Varsano, M.D., Dept. of Pulmonary Medicine, Sapir Medical Center, Meir General Hospital, Kfar-Sava 44281, Israel. E-mail: Varsanos{at}green.co.il
(Received in original form September 16, 1997 and in revised form March 4, 1998).
Acknowledgments: This research was supported by a grant from the M. Modan Cancer Research Fund, Tel-Aviv University, and by the Israel Cancer Association, with a grant donated by Ms. Fanni M. Shor in memory of her late husband Mouritz. The authors are grateful to Ms. Rachel Schickler and Ms. Bracha Gal for assistance with flow cytometry studies, and to Ms. Sara Gon-Paz for word processing.
Abbreviations CIP, complement inhibitory proteins; DAF, decay-accelerating factor; Dex, dexamethazone; FITC, fluorescein isothiocyanate; IFN, interferon; IL, interleukin; mAb, monoclonal antibodies; MCP, membrane cofactor protein; MFI, mean fluorescence intensity; PBS, phosphate-buffered saline; TNF, tumor necrosis factor.
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References |
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Materials and Methods
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Conclusions
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 D. R. Shafren, J. Gardner, V. H. Mann, T. M. Antalis, and A. Suhrbier Picornavirus Receptor Down-Regulation by Plasminogen Activator Inhibitor Type 2 J. Virol., September 1, 1999; 73(9): 7193 - 7198. [Abstract] [Full Text]
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