| Objective: PS-T has special anticancer effect and can obviously enhance immune function on patients of hepatoma, lung cancer, esophageal carcinoma, mammary cancer, cancer of colon, carcinoma of bladder, renal carcinoma, leukaemia and carcinoma of stomach, without having manifest side effect. While there was very few research on PS-T true mechanism of antitumor effect.Our study was undertaken to investigate its growth inhibiting effect and apoptosis induction. In this experiment, we use esophageal squamous carcinoma cell line Eca-109 to investigate the anticancer effect of PS-T and initially study its molecular mechanism of action. Our main object was to provide the experimental evidence of PS-T on the treatment of esophageal carcinoma.Methods: We detected growth inhibitory effect of PS-T on esophageal squamous carcinoma cell line Eca-109 with MTT assay in vitro and nude transplantation tumor model in vivo. Apoptosis was detected by Annexin V-FITC and DAPI dyeing methods. Cell cycle was detected by flow cytometry. Apoptosis protein of Bcl-2, Bax, Caspase-3 were detected on the nude transplantation tumor tissue by immunohistochemistry.Results: 1.The inhibition ratio of PS-T on esophageal squamous carcinoma cell line Eca-109 increase in dose-dependent manner. 2.The transplantation tumor weights of group A(control group) were significantlyhigher than those of group B(cisplatin group) > C(PS-T group) and D(combined group) (PO.01). The inhibitory rates of group B> C and D were 42.88%> 45.41% and 60.91% respectively, which indicated that PS-T had inhibitory effect on tumor. There was significant difference between group B> C and D (P<0.05), indicating that the combining drugs had synergistic effects. 3.Effect of PS-T on the toxic side effect of chemotherapy. At the end of this experiment, the weight of nude mice in group B and D decreased obviously than those of group A and C(P<0.01) ,with significant difference between group B and group D (P<0.05 ) .There was no difference between group A and group C(P>0.05). The results indicated that treatment with PS-T has no side effect. The toxic effect in combination group was significantly attenuated than that of cispiatin group. 4.The apoptotic rate of esophageal squamous carcinoma cell line Eca-109 treated with PS-T(4mg/ml ) at 48 hours was 11.4% by Annexin V-FITC methods. Morphological variations of apoptosis were observed at 48 hours treated with PS-T(4mg/ml ) by DAPI dyeing methods. 5. In control > cispiatin^ PS-T and combined group in vitro, the results of the cell cycle distribution by Flow cytometry showed that the cell ratio of Go/G! stage were 44.5°/^ 57.5%> 52.3% and 68.9% respectively, while that of S stage were 15.7%> 27.2%> 25.2% and 31.2%.The percentages of the cell of Go/Gi stage were increased with that of S stage decreased. 6. Immunohistochemical staining of Bcl-2 showed significant difference between group A and group B> C> D (PO.01), which indicated that PS-T could inhibit the expression of bcl-2 in tumor cells. 7.1mmunohistochemical staining of Bax showed significant difference between group A and group B> C> D (P<0.05), which indicated that PS-T could increase the expression of Bax in tumor cells. 8.Immunohistochemical staining of Caspase-3 showed significant difference between group A and group B> CU D (P<0.05), which indicated that PS-T couldincrease the expression of Caspase-3 in tumor cells.Conclusions: 1 .PS-T can inhibit the growth of esophageal squamous carcinoma cell line Eca-109 in vitro and the growth of transplantation tumor of esophageal squamous carcinoma cell line Eca-109 in nude mice. 2.PS-T can induce apoptosis of tumor cells in vitro. 3.PS-T can induce the apoptosis of tumor cells by inhibiting the expression of bcl-2 and increasing the expression of Bax> Caspase-3. 4.Unlike traditional chemotherapy medicines , PS-T has no toxic effect and can alleviate the toxic side effect of cisplatin.
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