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Response of L-1210 tumor in mice toward treatment with interferon or poly(I) X poly(C)
Abstract:
Two interferon (IFN)-mediated enzyme activities, the protein kinase and pppA(2'p5'A)n synthetase (2-5A synthetase) were employed to demonstrate the action of IFN on different tissues of mice as well as in ascitic tumors of L-1210 IFN (alpha + beta)-sensitive (L-1210S) and IFN-resistant (L-1210R) leukemia cells. The protein kinase is manifested by the phosphorylation of endogenous protein of molecular weight 67 kD (p67K kinase). Control and L-1210R or L-1210S tumor-bearing mice were found to respond similarly to treatment with IFN or when injected with an IFN inducer, poly(I) X poly(C). The 2-5A synthetase and the p67K kinase were enhanced in the lung and the spleen of mice, both control and with tumor graft. There was no apparent effect on L-1210R leukemia cells whereas in L-1210S cells the level of both enzymes was enhanced in response to treatment of mice with IFN or poly(I) X poly(C). These results indicate that the presence of tumor cells did not trigger modifications in the response of mice toward treatment with IFN. Furthermore, they provide biochemical evidences to show the response of IFN-sensitive and IFN-resistant tumor cells during treatment of the host with IFN.
Insights
Interferon (IFN) treatment enhances key enzyme activities in mouse tissues and IFN-sensitive leukemia cells, but not IFN-resistant cells. Tumor presence did not alter the host
Area of Science:
- Immunology
- Biochemistry
- Molecular Biology
Background:
- Interferons (IFNs) are crucial signaling proteins in the immune system.
- IFN-mediated enzyme activities, including protein kinase and 2-5A synthetase, are key to IFN's biological effects.
- Understanding IFN action in different tissues and tumor cells is vital for therapeutic applications.
Purpose of the Study:
- To investigate the action of interferon (IFN) on mouse tissues and L-1210 leukemia cells.
- To assess the impact of IFN on IFN-sensitive (L-1210S) and IFN-resistant (L-1210R) leukemia cells.
- To evaluate the role of IFN-induced enzymes, p67K kinase and 2-5A synthetase, in response to IFN treatment.
Main Methods:
- Measuring protein kinase and 2-5A synthetase activities in various mouse tissues and L-1210 leukemia cells.
- Administering IFN or poly(I) X poly(C) (an IFN inducer) to control and tumor-bearing mice.
- Analyzing enzyme activity in lung, spleen, and leukemia cells (L-1210S and L-1210R).
Main Results:
- IFN treatment and poly(I) X poly(C) administration enhanced 2-5A synthetase and p67K kinase in mouse lung and spleen.
- These enzyme activities were significantly increased in IFN-sensitive L-1210S leukemia cells.
- No significant changes in enzyme activities were observed in IFN-resistant L-1210R leukemia cells.
Conclusions:
- The presence of tumor cells did not modify the host's response to IFN treatment.
- Biochemical evidence demonstrates differential responses of IFN-sensitive and IFN-resistant tumor cells to host IFN therapy.
- These findings highlight the importance of cellular sensitivity in determining the efficacy of IFN-based treatments.