PURPOSE
Retinoic acid is a substance that has previously been reported to increase radiosensitivity, but at concentrations likely to inhibit cell growth or to induce celluar differentiation. We choose head and neck cancer cell lines to investigate the role of retinoic acid as a radiosensitizer and to elucidate the mechanism through the changes in the expression of retinoid receptors and squamous cell differentiation marker.
MATERIALS AND METHODS
Three cell lines (PCI-50, SqCC/ Y1 and UMSCC-11B) were used. 7-AAD staining for apoptosis and Western blot analysis for RAR-alpha, beta, gamma, RXR-alpha, beta, gamma and involucrin were performed after various treatments (control, beta-all-trans-retinoic acid (t-RA) only (10 6 M), radiation only (3 Gy), radiation with t-RA).
RESULTS
The synergistic radiosensitivity effect of t-RA was seen only radioresistant UMSCC-11B cell line. Expression of RAR-beta was induced by t-RA in maily UMSCC- 11B cell line. RAR-alpha,gamma, and RXR-alpha, beta, gamma expression were not changed in all cell lines tested. Expression of involucrin was inhibited by t-RA in PCI-50 cell line but other two cell lines were not changed by t-RA treatment.
CONCLUSION
We found that only radioresistant cell line (UMSCC-11B) showed synergistic radiosensitivity effect by t-RA and this mechanism may be through RAR-beta expression induction.