Retinoic Acid as a Radiosensitizer on the Head and Neck Squamous Cell Carcinoma Cell Lines |
Jae Hong Seo, Kap No Lee, Sun Hee Park, Chul Won Choi, Byung Soo Kim, Sang Won Shin, Yeul Hong Kim, Jun Suk Kim |
1Department of Internal Medicine, Korea University School ofMedicine, Seoul, Korea. 2Department of Clinical Pathology, Korea University School ofMedicine, Seoul, Korea. 3Department of Graduate School of Medicine, Korea UniversitySchool of Medicine, Seoul, Korea.
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Published online: August 31, 2001. |
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ABSTRACT |
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. |
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