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Antiproliferative effects of interleukin-1 alpha and nitric oxide release in a human ovarian carcinoma cell line
1UNIV MILAN,INST PHARMACOL,APPL PHARMACOL SECT,I-20129 MILAN,ITALY.
Abstract:
Interleukin-1 (IL-1) exerts direct antiproliferative effects on a number of human tumor cell lines, but the mechanisms involved are still poorly understood. Nitric oxide (NO) has been shown to mediate some of the actions of IL-1. Therefore, we investigated the role played by NO in the cytostatic effects of IL-1 alpha on NIH:OVCAR-3 cells, a cell line which has been shown to possess IL-1 receptors and to respond to the cytokine with growth arrest; the involvement of NO release in the synergistic interaction between IL-1 alpha and adriamycin (ADR) observed in this cell line was also studied. 72 h exposure to concentrations of IL-1 alpha similar to its IC50 value, were found to enhance NO release. This was significantly reduced by co-incubation with 1 mM L-NAME, which however did not significantly affect the IC50 values, either for IL-1 alpha or for the combination IL-1 alpha:ADR (1:20,000). We conclude that induction of NO synthesis in IL-1 alpha-treated cells is probably a side effect originating from transcription factor activation by the cytokine, and that neither the antiproliferative effects of IL-1 alpha nor its potentiation of ADR cytotoxicity depend on NO release.
Insights
Interleukin-1 alpha (IL-1α) can inhibit tumor cell growth, but nitric oxide (NO) does not mediate this effect. NO release in IL-1α-treated cells appears to be a side effect, not crucial for IL-1α
Area of Science:
- Immunology
- Molecular Biology
- Cancer Research
Background:
- Interleukin-1 (IL-1) exhibits antiproliferative effects on human tumor cell lines.
- Nitric oxide (NO) is implicated in mediating some IL-1 actions.
- The precise mechanisms underlying IL-1's antiproliferative effects remain unclear.
Purpose of the Study:
- To investigate the role of NO in the cytostatic effects of IL-1 alpha on NIH:OVCAR-3 cells.
- To determine if NO mediates the synergistic interaction between IL-1 alpha and adriamycin (ADR).
Main Methods:
- NIH:OVCAR-3 cells were exposed to IL-1 alpha.
- Nitric oxide (NO) release was measured.
- The effect of L-NAME (a NO synthesis inhibitor) on IL-1 alpha and IL-1 alpha:ADR cytotoxicity was assessed.
Main Results:
- IL-1 alpha exposure enhanced NO release in NIH:OVCAR-3 cells.
- L-NAME significantly reduced NO release but did not alter the IC50 values for IL-1 alpha or the IL-1 alpha:ADR combination.
- The antiproliferative effects of IL-1 alpha and its synergy with ADR were not dependent on NO.
Conclusions:
- NO synthesis induction in IL-1 alpha-treated cells is likely a byproduct of transcription factor activation.
- NO release is not essential for the antiproliferative actions of IL-1 alpha.
- NO does not mediate the potentiating effect of IL-1 alpha on adriamycin cytotoxicity.
