Studys On The Anticancer Activity Of HS-1, A Bioactive Compound From A Chinese Medicinal Herb, CD

This paper focused on the study of the in vitro anticancer activity of HS-1, a bioactive compound from a Chinese medicinal herb, CD.The proliferation of the cells of K562 (the Chronic Myeloid Leukemia Cell Line),HCT-15 (the Human Colorectal Adenocarcinoma Cell Line, A549 (the Lung Alveolar Epithelial Cell Line), A431 (the Human Squamous Carcinoma Cell Line) and MCF-7 (the Human Breast Cancer Cell Line) was inhibited by HS-1 in a dosage dependent manner, while the higher concentration of CDDP was required to the same inhibitory effect. HS-1 changed the cell cycles, and thus induced apoptosis. The reduction of mitochondrial membrane potential which often takes place in the apoptotic cells was also found in the cells treatment with HS-1; And "DNA ladder" achieved from the cells treated by HS-1 meant that HS-1 could be regarded as a apoptosis inducer.The proliferation of more A2780/CDDP cells, the CDDP-resistant A2780 (the Cell Line of the Human Ovarian Cancer) cells, than their parental cellswas inhibited by HS-1, and the Resistence Factor was 0.678. The inhibitory effect of the classical anticancer drugs CDDP, DOXORUBICIN and MITOMYCIN C on A2780/CDDP cells was worse than on A2780 cells, and the Resistance Factors of the two kind cells treatment with those drugs were over 2.5. VINCRISTINE which had the similar Resistance Factor with HS-1, had to be used at a higher concentration to the same effect. We examined the P-glycoprotein, which often develops multidrug resistance, but A2780/CDDP was a P-glycoprotein-negative cell line, and the hypothesis that HS-1 might have an effect on P-glycoprotein was not proved. More A2780/CDDP cells than A2780 cells were arrested at G0/G1 in the cells treatment with HS-1, while CDK4, cyclin D1, p53 and p21, the proteins at G0/G1, had not remarkable changement. The A2780 and A2780/CDDP cells both were found to apoptosis after treatment with HS-1, but caspase-3, PARP was not cut. No changement of Bcl-2, Bax and caspase-9 in these two kind cells treatment with HS-1 meant that the reduction of the mitochondrial membrane potential of these two kind cells might be the subsequent effect of the apoptosis of the cells. All these resulted that HS-1 might affect the cells in a special way.To study the toxicity of HS-1 to normal cells, mouse marrow stromal colony cells were selected. In accordings to CDDP, HS-1 prohibited the proliferation of mouse marrow stromal colony cells in a dosage and time dependent manner, so we conluded that HS-1 was not fatal to marrow and its toxicity may be eliminated or minimized by choosing an appropriate dosage and time for treatment.