Thermal resistance of human malignant melanoma modulated by prostaglandin E2.
The inhibition of DNA synthesis in a human malignant melanoma cell line as measured by tritiated thymidine (3H-TdR) incorporation was both time- and temperature dependent. Two components of cell damage were identified: a cytostatic, temporary component from which cells recovered within 2-6 days, and a cytotoxic, permanent component from which no recovery was observed. Thermotolerance was induced in M14 cells by sublethal heat treatment at 41 degrees C for 1 hr. However, induction of thermotolerance was blocked by indomethacin, a prostaglandin synthetase inhibitor. Exogenous PGE2 at concentrations up to 10 micrograms/ml also protected cells from heat damage. These data suggest that prostaglandin synthesis increases during heat stress and may play a role in protecting cells from thermal damage.
Surgical Services, Veterans Administration Medical Center, Sepulveda, California.
D H
DH
Kern
D N
DN
Krag
G L
GL
Kauffman
D L
DL
Morton
F K
FK
Storm
D015232:Dinoprostone; D006358:Hot Temperature / Q000627:therapeutic use*; D006801:Humans; D066298:In Vitro Techniques; D008545:Melanoma / Q000378:metabolism / Q000628:therapy*; D011458:Prostaglandins E / Q000502:physiology*; D014407:Tumor Cells, Cultured; D014410:Tumor Stem Cell Assay
D011458:Prostaglandins E; D015232:Dinoprostone