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J Korean Cancer Assoc. 2000 Aug;32(4):783-792. Korean. In Vitro.
Kim SJ , Paek CW , Seo JH , Choi CW , Kim BS , Shin SW , Kim YH , Kim JS , Kim A , Lee KN , Kim SH , Choi G , Yoo YA .
Departments of Internal Medicine, Korea University School of Medicine, Seoul Korea.
Departments of Pathology, Korea University School of Medicine, Seoul Korea.
Departments of Clinical Pathology, Korea University School of Medicine, Seoul Korea.
Departments of Surgery, Korea University School of Medicine, Seoul Korea.
Departments of Otolaryngology, Korea University School of Medicine, Seoul Korea.
Departments of Graduate School of Biotechnology, Korea University School of Medicine, Seoul Korea.
Abstract

PURPOSE: Retinonic acid (RA) has been reported to induce differentiation and growth inhibition in various head and neck squamous cancer cell (HNSCC) lines. We hypothesized that this growth inhi bition might be explained by RA-induced apoptosis on cell cycle arrest mechanism. Therefore, we studied the degree of RA-induced apoptosis with variable RA concentration and exposure duration. MATERIAL AND METHODS: The flow cytometric evaluation of apoptosis degree and cell cycles were carried out with 7-amino actinomycin D (7AAD) and propium iodide (PI) respectively, with var ious RA exposure durations (2, 3, 6 day) and concentrations (conrol, 10 6, 10 7, 10 8, 10 9, 10 10 mole). Two different HNSCC lines (1483, SqCC/Y1) were used and the experiment was repeated twice. RESULTS: The maximal fraction of apoptosis in 1483 and SqCC/Y1 cell lines were observed at same concentration and exposure duration (1483: 6th day & 10 6, mole, and SqCC/Y1: 6th day & 10 6 mole). In our experimental model, RA did not induce specific cell cycle arrest in these HNSCC lines. However we observed S phase fraction increase in SqCC/Y1 cell line after RA treatment. CONCLUSION: We suppossed that in HNSCC lines, RA-induced cell growth inhibition could be explained by not only RA-induced apoptosis but also cell cycle arrest. Futher, in vitro study has been carried out to elucidate the RA-iduced cell growth inhibition mechanism in our laboratory.

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