J Korean Cancer Assoc.
2000 Aug;32(4):783-792.
The Mechanism of Retinoic Acid-induced Growth Suppression
in Head and Neck Squamous Cancer Cell Lines
- Affiliations
-
- 1Departments of Internal Medicine, Korea University
School of Medicine, Seoul Korea.
- 2Departments of Pathology, Korea University
School of Medicine, Seoul Korea.
- 3Departments of Clinical Pathology, Korea University
School of Medicine, Seoul Korea.
- 4Departments of Surgery, Korea University
School of Medicine, Seoul Korea.
- 5Departments of Otolaryngology, Korea University
School of Medicine, Seoul Korea.
- 6Departments 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.