Cancer Research and Treatment

Original Articles

The Mechanism of Retinoic Acid-induced Growth Suppression in Head and Neck Squamous Cancer Cell Lines: Seok Jin Kim, Chang Won Paek, Jae Hong Seo, Chul Won Choi, Byung Soo Kim, Sang Won Shin, Yeul Hong Kim, Jun Suk Kim, Aree Kim, Kap No Lee, Sun Han Kim, Geon Choi, Young A Yoo; J Korean Cancer Assoc. 2000;32(4):783-792.

Abstract PDF: 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.

Genistein Induced Inginition of Cell Proliferation and Programmed Cell Death in the Human Cancer Cell Lines: Young Hyun Choi, Soo Jae Lee, Min Kim, Lijuan Zhang, Won Ho Lee, Kun Young Park; J Korean Cancer Assoc. 1998;30(4):800-808.

Abstract PDF: PURPOSE
Genistein, a natural isoflavonoid phyto-oestrogen present in plant foods including citrus fruits and soybean, is a specific inhibitor of tyrosine kinase and topoisomerase II. In this paper we examined the effect of genistein on cell cycle progression and programmed cell death in the human prostate carcinoma PC-3 and Ewing's sarcoma CHP-100 cells. MATERIAL AND METHODS: Effect of genistein on cell cycle was measured by DNA flow cytometric analysis. In order to understand anticancer effect of genistein on cell cycle, Western blot analysis, immune complex kinase assay, DAPI staining and DNA fragmentation analysis were conducted.
RESULTS
DNA flow cytometric analysis indicated that genistein induced cell cycle arrest at the G2/M transition phase. Western blot analyses showed that genistein selectively reduced expression of cyclin B1 and cdk2-dependent kinase activity in both cell lines. Genistein also induced apoptosis that was demonstrated by direct visualization of morphological nuclear changes and confirmed by the production of characteristic ladder patterns of genomic DNA fragmentation.
CONCLUSION
The chemopreventive activity of genistein is proven to be related with the induction of cell cycle arrest at the G2/M transition phase by reducing the expression of cyclin B1 and cdk2-dependent kinase activity, and also with the induction of apoptosis in the tested cancer cells.

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