抑癌素M的基因克隆及其在大肠杆菌中的表达

应用ＰＣＲ技术制备了抑癌素Ｍ的全基因ＤＮＡ顺序，将其克隆到表达载体ｐＳＰ质粒上，并转化进大肠杆菌宿主细胞ＪＭ１０３构建成工程菌。该工程菌经诱导表达后，经ＳＤＳ电泳和薄层扫描测定，表明表达量可达３５％。经初步提纯后进行细胞活性测定，表明其抑制黑色素瘤细胞的活性为１２ＧＩＡ／ｎｇ蛋白。

菝葜抑癌素的抗癌作用及其机制研究

探讨菝葜制瘤素对不同类型癌细胞的抑制作用及其可能的分子机制。方法 采用标准MTT法检测菝葜抗癌活性因子对人A549肺癌细胞、MCF-7人乳腺癌细胞、HCT116结肠癌细胞、人肝癌HepG2细胞增殖的抑制作用;流式细胞仪可检测菝葜制瘤素对癌细胞凋亡的抑制作用。结果 菝葜制瘤素能显着抑制四种癌细胞的增殖,且具有一定的浓度和时间依赖性;菝葜制瘤素可诱导四种癌细胞凋亡,且随浓度增加,凋亡率增加。 结论 菝葜制瘤素具有广泛的抗癌作用,其机制可能与诱导癌细胞凋亡有关。

食管鳞癌组织中抑癌基因SEMA3B的表达及意义

目的探讨抑癌基因信号素3B(SEMA3B)在食管鳞癌(ESCC)发生、发展中的作用。方法采用RT-PCR法检测51例食管鳞癌组织(观察组)及相应正常食管组织(对照组)中SEMA3B基因的表达,并分析其与食管鳞癌临床病理参数的关系。结果对照组SEMA3B基因均表达,观察组SEMA3B基因表达缺失率为58.8%(30/51,P<0.05);SEMA3B基因表达与食管鳞癌组织发生部位、淋巴结转移和临床病理分期有关,而与年龄、性别、肿瘤细胞分化程度和大体分型无关。结论SEMA3B基因的表达异常可能在食管鳞癌的发生、发展及预后中起重要作用;SEMA3B可作为反映食管鳞癌生物学行为的指标之一。

Long acting octreotide in the treatment of advanced hepatocellular cancer and overexpression of somatostatin receptors: Randomized placebo-controlled trial

AIM: To estimate if and to what extent long acting octreotide (LAR) improves survival and quality of life in patients with advanced hepatocellular carcinoma (HCC). METHODS: A total of 127 cirrhotics, stages A-B, due to chronic viral infections and with advanced HCC, were enrolled in the study. Scintigraphy with 111Indium labeled octreotide was performed in all cases. The patients with increased accumulation of radionuclear compound were randomized to receive either oral placebo only or octreotide/octreotide LAR only as follows: octreotide 0.5mg s.c. every 8 h for 6 wk, at the end of wk 4-8 octreotide LAR 20 mg i.m. and at the end of wk 12 and every 4 wk octreotide LAR 30mg i.m.. Follow-up was worked out monthly as well as the estimation of quality of life (QLQ-C30 questionnaire). Patients with negative somatostatin receptors (SSTR) detection were followed up in the same manner. RESULTS: Scintigraphy demonstrated SSTR in 61 patients. Thirty were randomized to receive only placebo and 31 only octreotide. A significantly higher survival time was observed for the octreotide group (49 ± 6 wk) as compared to the control group (28 ± 1 wk) and to the SSTR negative group (28 ± 2 wk), LR = 20.39, df = 2, P < 0.01. The octreotide group presented 68.5% lower hazard ratio [95% CI (47.4%-81.2%)]. During the f irst year, a 22%, 39% and 43% decrease in the QLQ-C30 score was observed in each group respectively.CONCLUSION: The proposed therapeutic approach has shown to improve the survival and quality of life in SSTR positive patients with advanced HCC.

Inhibitory effects of N-(4-hydrophenyl) retinamide on liver cancer and malignant melanoma cells

AIM: To investigate the effect of N-(4-hydrophenyl) retinamide (4-HPR), the derivative of retinoic acid, on inhibition of migration, invasion, cell growth, and induction of apoptosis in hepatocellular carcinoma cells (HCCs) and malignant melanoma cells.METHODS: 4-HPR was chemically synthesized. Cellular migration and invasion were assayed by Borden chamber experiment. Cell growth was assayed by MTT chromometry.Apoptosis effect was measured using Hoechst 32258 staining and flow cytometry. Gene transfection was performed with lipofectamine.RESULTS: We observed that the migration of HCC and melanoma cells was significantly suppressed by 4-HPR and the migration cells were reduced to 58±5.03 (control 201±27.2, P＜0.05, n = 4) in SMMC 7721-k3 HCC, and to 254±25.04 (control 302±30.1, P＜0.05, n = 4) in melanoma cells after 6-h incubation with 4-HPR. The invasion through reconstituted basement membrane was also significantly reduced by 4-HPR treatment to 11.2±3.3 in SMMC 7721-k3 HCC (control 27±13.1), and to 24.3±3.2 in melanoma cells (control 67.5±10.1, P＜0.05, n = 3). Cell growth, especially in melanoma cells, was also significantly inhibited.Furthermore, 3 μmol/L of 4-HPR induced apoptosis in B16 melanoma cells (37.11±0.94%) more significantly than all-trans retinoic acid (P＜0.05), but it failed to induce apoptosis in SMMC 7721-k3 HCC. The mechanism for 4-HPR-induced apoptosis was not clear, but we observed that 4-HPR could regulate p27kip1, and overexpression of cerebroside sulfotransferase (CST) diminished the apoptosis induced by 4-HPR in melanoma cells.CONCLUSION: 4-HPR is a potent inhibitor of HCC migration and inducer of melanoma cell apoptosis. CST and p27kip1 expression might be associated with 4-HPR-induced apoptosis.

Inhibitory effect of schisandrin B on gastric cancer cells in vitro

AIM： To investigate the inhibitory effect and possible mechanism of action of schisandrin B in SC-B on gastric cancer cells in vitro.METHODS： SC-B consisted of schisandrin B, aloeemodin, and Astragalus polysaccharides. Exponentially growing human gastric cancer SGO7901 cells were divided into six treatment groups： （1） control group （RPMI 1640 medium）; （2） negative control group （2% DMSO）; （3） positive control group （50 mg/L 5-Fluorouracil, 5-FU）; （4） low-dose group （LSC, final concentration of schisandrin B, 25 mg/L）, （5） moderate-dose group （MSC, final concentration of schisandrin B, 50 mg/L）; （6） highdose group （HSC, final concentration of schisandrin B, 100 mg/L）. Follow-up was done at 12-48 h. An MTT （Methylthiazolyldiphenyl-tetrazolium bromide） assay was used to examine the inhibitory effect of SOB on gastric cancer cells. The mitosis index was assessed using an inverted microscope. Flow cytometry was used to visualize the cell cycle. An RT-PCR （Reverse transcription-Polymerase chain reaction） -based assay was used to detect mRNA expression for cyclin D1 and glyceraldehyde-3-phosphate dehydrogenase （GAPDH）.RESULTS： The MTT assay showed that the number of living cells in the LSC, MSC and HSC groups was significantly smaller than that in the DMSO-treated group （P 〈 0.05） at 12-48 h. The inhibitory rate （IR） of the LSC group was 41.15% ± 3.86%, 59.24% ± 5.34% and 69.93% ± 7.81% at 12, 24 and 48 h, respectively. The IR of the MSC group was 42.82% ± 4.94%, 62.68% ± 7.58% and 71.79% ± 8.12% at 12, 24 and 48 h, respectively. The IR of the HSC group was 37.50% ± 3.21%, 40.34% ± 2.98% and 61.99% ± 4.88% at 12, 24 and 48 h, respectively. These results suggested that a moderate dosage had the most obvious inhibitory efficacy at 48 h. Compared to the DMSO group, the mitosis index of the LSC, MSC, HSC groups was greatly decreased （P 〈 0.05） at all time points. Any dose of SC-B suppressed mitosis within 12-48 h. Compared to the DMSO group, the percentage of cells in the G0/G1 phase of the MSC group was greatly increased, and that of the S ＋ G2M phase was greatly decreased, while the percentage of cell inhibition （PCI） in the MSC group was greatly increased （P 〈 0.05）. This suggested that SC-B could exclusively arrest cells in the G0/G1 phase. Cyclin D1 mRNA expression was lower in the MSC group than that in the DMSO group （P 〈 0.05）.CONCLUSION： SC-B can inhibit the proliferation and aberrant mitosis of human gastric cancer SCG-7901 cells /n v/tro, This inhibitory effect may be due to the down- regulation of cyclin D1 mRNA expression, which causes cell cycle arrest of gastric cancer cells.

Combined treatment of vitamin K_2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis

Although it is well known that the hepatocellular carcinoma (HCC) is an ominous complication in patients with liver cirrhosis, there has been no approved drug to prevent the development of HCC to date. We previously reported that the combined treatment of vitamin K2 (VK) and angiotensin-converting enzyme inhibitor (ACE-I) significantly suppressed the experimental hepatocarcinogenesis. A 66-year-old Japanese woman with hepatitis C virus (HCV)-related liver cirrhosis developed a dysplastic nodule in the liver detected by enhanced computed tomography along with elevation of the tumor markers, namely, alpha-fetoprotein (AFP) and lectin-reactive demarcation (AFP-L3), suggesting the presence of latent HCC. After oral administration of VK and ACE-I, the serum levels of both AFP and AFP-L3 gradually decreased without any marked alteration of the serum aminotransferase activity. After one-year treatment, not only the serum levels of AFP and AFP-L3 returned to the normal ranges, but also the dysplastic nodule disappeared. Since both VK and ACE-I are widely used without serious side effects, this combined regimen may become a new strategy for chemoprevention against HCC.

Effect of perioperative blood transfusion on clinical outcomes in hepatic surgery for cancer

Allogeneic blood transfusion during liver resection for malignancies has been associated with an increased incidence of different types of complications: infectious complications, tumor recurrence, decreased survival. Even if there is clear evidence of transfusion-induced immunosuppression, it is difficult to demonstrate that transfusion is the only determinant factor that decisively affects the outcome. In any case there are several motivations to reduce the practice of blood transfusion. The advantages and drawbacks of different transfusion alternatives are reviewed here, emphasizing that surgeons and anesthetists who practice in centers with a high volume of liver resections, should be familiar with all the possible alternatives.

Neuroendocrine gastric carcinoma expressing somatostatin: A highly malignant, rare tumor

Poorly differentiated gastric neuroendocrine carcinomas, although rare, deserve particular attention, as they are aggressive and have an extremely poor prognosis. In this report we describe a gastric neuroendocrine carcinoma with rapidly fatal outcome. Immunohistological staining of the resected specimens revealed that the tumor was an endocrine carcinoma. The tumor disclosed intense immunoreactivity to pan-neuroendocrine markers and diffuse somatostatin immunoreactivity. There were no psammoma bodies and no demonstrable association with yon Recklinghausen＇s neurofibromatosis. In the gastrointestinal tract, neuroendocrine tumors producing predominantly somatostatin have been described only in the duodenum. To the best of our knowledge, the present report is the second case report of a neuroendocrine gastric carcinoma expressing diffusely somatostatin as the only neuroendocrine regulatory peptide.

Relationship between expression of gastrin, somatostatin,Fas/FasL and caspases in large intestinal carcinoma

AIM: To explore the correlation between the mRNAs and protein expression of gastrin (GAS), somatostatin (SS) and apoptosis index (AI), apoptosis regulation gene Fas/ FasL and caspases in large intestinal carcinoma (LIC). METHODS: Expression of GAS and SS mRNAs were detected by nested RT-PCR in 79 cases of LIC. Cell apoptosis was detected by molecular biology in situ apoptosis detecting methods (TUNEL). Immunohistochemical staining for GAS, SS, Fas/FasL, caspase-3 and caspase-8 was performed according to the standard streptavidin-biotin-peroxidase (S-P) method. RESULTS: There was a significant positive correlation between mRNA and protein expression of GAS and SS (GASrs=0.99, P < 0.01; SSrs = 0.98, P < 0.01). There was significant difference in positive expression rates of GAS, SS mRNAs and protein among different histological differentiation, histological types and Dukes’ stage of LIC. The AI in GAS high and moderate expression groups was significantly lower than that in low expression groups (3.75 ± 2.38 vs 7.82 ± 2.38, P < 0.01; 5.51 ± 2.66 vs 7.82 ± 2.38, P < 0.01), and the AI in SS high and moderate expression groups was significantly higher than that in low expression groups (9.03 ± 1.76 vs 5.35 ± 3.00, P < 0.01; 7.44 ± 2.67 vs 5.35 ± 3.00, P < 0.01). There was a significant negative correlation between the integral ratio of GAS to SS and the AI (rs = -0.41, P < 0.01). The positive expression rate of FasL in GAS high and moderate expression groups was higher than thatin low expression group (90.9% and 81.0% vs 53.2%, P < 0.05). The positive expression rates of Fas, caspase-8 and caspase-3 in SS high (90.0%, 90.0% and 100%) and moderate (80.0%, 70.0%, 75.0%) expression groups were higher than that in low expression group (53.1%, 42.9%, 49.0%) (90.0% and 80.0% vs 53.1%, P < 0.05; 90.0% and 70.0% vs 42.9%, P < 0.05; 100.0% and 75.0% vs 49.0%, P < 0.05). There was a significant positive correlation between the integral ratio of GAS to SS and the semiquantitative integral of FasL (rs = 0.32, P < 0.01). CONCLUSION: GAS and SS play important roles in the regulation and control of cell apoptosis in LIC, and the mechanism may be directly related to the aberrant expression of Fas/FasL. The GAS and SS will be valuable targets of the biological behavior of LIC.

Genetic Basis of Gastric Cancer

Gastric cancer is the result of multiple risk factors,including environmental factors,genetic factors and the interaction between them.The environmental factors mainly include dietary,Helicobacter pylori infection and family history of gastric cancer.Genetic factors mainly refer to the susceptible genes that cause epigenetic alterations in oncogenes,tumor suppress genes,cell cycle regulators,DNA repair genes and signaling molecules.This paper summarizes the susceptible genes of gastric cancer and explores the genetic basis of it.

The anti-cancer effect of Huaier aqueous extract with rh-Endostatin and DDP

Objective: The aim of our study was to explore the inhibition and apoptosis-inducing effect of the combination of Huaier aqueous extract with recombinant human Endostatin and DDP in human lung adenocarcinoma A549 cells. We also investigated the reversal effect of Huaier aqueous extract in reversing cisplatin resistance in human lung adenocarcinoma A549/DDP cells. Methods: We treated A549 cells with Huaier aqueous extract and the combination of Huaier aqueous extract and DDP or rh-Endostatin for 24 h, 36 h and 48 h. And then we calculated the inhibition rate through MTT approach and detected the apoptosis rate by flow cytometry. We also treated A549 and A549/DDP cells with DDP, Huaier aqueous extract, DDP and Huaier aqueous extract for 72 h, respectively. Results: Huaier aqueous extract can inhibit the growth of A549 cells and the inhibition rate improved with the increase of the concentration. The inhibition rate of the combination of rh-Endostatin and 4 mg/mL of Huaier aqueous extract in three time points and the combination of rh-Endostatin and 2 mg/mL of Huaier aqueous extract in the time point of 48 h on the growth of A549 cells all improved(P < 0.005). The inhibition rate of the combination of DDP and Huaier aqueous extract with the concentration of 2 mg/mL or 4 mg/mL on the growth of A549 cells all improved(P < 0.005). The combination of Huaier aqueous extract and DDP and the combination of Huaier aqueous extract with rh-Endostatin and DDP can improve the inhibition on the growth of A549 cells(P < 0.005). Conclusion: Huaier aqueous extract has the inhibition and apoptosis-inducing effects on the A549 cells. And the combination of Huaier aqueous extract and rh-Endostatin or DDP has the synergistic effects on the inhibition of A549 cells. The combination of Huaier aqueous extract with rh-Endostatin and DDP has the synergistic effects on the inhibition of A549 cells. Huaier aqueous extract can reverse the cisplatin resistance in human lung adenocarcinoma A549/DDP cells.

Reversal effect of recombinant human Endostatin on cisplatin resistance in A549/DDP human lung adenocarcinoma cells in vitro

Objective： Recombinant human Endostatin （rh-Endostatin, YH-16） can reverse cisplatin resistance in A549/DDP cells. However, the possible effect of rh-Endostatin in reversing DDP-resistance in A549/DDP cells and the mechanism are needed to be investigated. Methods： Lung adenocarcinoma cell line A549 and its DDP-resistant cell line A549/DDP were treated with DDP and/or recombinant human Endostatin. Difference in drug resistance was analyzed between different regi- mens and between different cell lines after a 72 h-treatment in vitro. And below the non-cytotoxic concentration of rh-End- ostatin, the possibility of rh-Endostatin in reversing DDP-resistance in A549/DDP was evaluated. The resistance protein which was detected in the study included P glycoprotein （P-gp） and topoisomerase II （Topo-II）. Results： Rh-Endostatin below 400 IJg/mL showed no cytotoxicity in either A549 or A549/DDP after 72 h-treatment with it. The inhibited concentration of 50% （IC50） observed for DDP was （0.79 _＋ 0.05） IJg/mL in A549 and （13.2 ＋ 1.1） in A549/DDP respectively. IC50 was reduced to 2.57 ＋ 0.05 #g/mL in A549/DDP treated by rh-Endostatin below the non-cytotoxic concentrations in combination with DDP, with a reversal fold （RF） of 5.14 and a relative reversal rate of 85.6%. Apoptotic rates were 2.01%, 13.47% and 29.26% re- spectively for cells treated with rh-Endostain, DDP, and the combination. The rate of the A549/DDP control group was 0.99%. The expression level of P-gp or Topo-II was higher in A549/DDP cells than in A549 cells. Rh-Endostatin may partially reverse DDP-resistance in A549/DDP cells in vitro, with a probable mechanism related to lowering expression of P-gp and Topo-II. Conclusien： Rh-Endostatin of non-cytotoxic dose partially reversed cisptatin resistance in cisplatin-resistant human lung adenocarcinoma cell line A549/DDP. Rh-Endostatin reversed the resistance of A549/DDP cells to DDP, which may be related to decreased protein expression of P-gp and Topo-II in A549/DDP cells.

Expression change of nuclear receptor corepressor (NCoR) in androgen independence prostate cancer and its clinical significance

Objective：To explore the expression of nuclear receptor corepressor （NCoR） in androgen independence prostate cancer （AIPC） and its clinical significance. Methods：The expression of NCoR and androgen receptor （AR） in prostatie tissues, from 15 cases with AIPC, 20 cases with androgen dependence prostate cancer （ADPC） and 20 cases with benign prostatic hyperplasia （BPH）, was detected by immunohistoehemistry respectively. Results：The expression of NCoR was observed mainly in the nucleus and slightly in the nucleus. The positive cell percentage of NCoR in AIPC was significantly lower than that in ADPC and BPH （P〈0. 01）. The NCoR expression was significantly lower in low differentiation prostate cancer （Pca） than that in high differentiation Pca （P〈0. 05）. The rate of NCoR expression was significantly higher in low stage Pca than that in high stage Pca （P〈0. 05）. AR, expressing in the nucleus, was found to be negative in one case of AIPC, while was strongly expressed in other cases of AIPC, and all eases of ADPC and BPH. Conclusion： The transition to AIPC of Pea may be correlated with the decrease of NCoR protein.

EFFECT OF SOMATOSTATIN ON THE CELL CYCLE OF HUMAN GALLBLADDER CANCER CELL

Objective To explore the effect of somatostatin on the cell cycle of human gallbladder cancercell. Methods Growth curve of gallbladder cancer cell was measured after somatostatin treated on gradientconcentration. Simultaneously, the change of gallbladder cancer cell cycle was detected using flow cytometry.Results Concentration-dependent cell growth inhibition caused by somatostatin was detected in gallbladder cancercell(P <0. 05). Cell growth was arrested in S phase since 12h after somatostatin treated, which reached its peak at24h, then fell down. The changes in apoptosis index of gallbladder cancer cell caused by somatostatin correlatedwith that’s in cell cycle. Conclusion Somatostatin could inhibit the cell growth of human gallbladder cancer cellin vitro on higher concentration. It might result from inducing growth arrest in S phase in early stage and inducingapoptosis in the late stage.

The Effect of calmodulin antagonist berbaminederivative-EBB on hepatoma in vitro and in vivo

OBJECTIVE: To evaluate the anti-hepatoma effect of Calmodulin antagonist 0 - 4-ethoxyl-butyl-Berbamine (EBB), one of the berbamine derivatives. METHODS: Monotetrazolium (MTT) method was used to analyze the effect of EBB on the proliferation and growth inhibition effect. Of a hepatoma cell line in vitro. A mouse hepatoma model was induced by injection of hepatoma cells (H22) in the abdominal cavity. The effect of EBB on survival at different concentrations as well as in combination with 5-FU were investigated in vivo. Flow cytometry analysis, dot blot hybridization, western blot, immunochemistry, enzyme-linked lectin assay (ELISA), trifluoperazine (TFP) and electron microscopic observation were used to study the effect of EBB on cell cycle process, P53 mRNA and protein levels, calmodulin content and ultrastractural changes of hepatoma cells. RESULTS: EBB exerts a very strong inhibitory effect on human hepatoma cell line 7402 and mouse hepatoma cell line H22 in vitro. The IC(50) value of EBB for the two cell lines are 3.312 microg/ml and 1.167 microg/ml, respectively. The sensitivity of H22 cells to 5-FU can be markedly enhanced: The IC(50) dosage of 5-Fu can be decreased from 0.75 microg/ml down to 0.15 microg/ml, when jointly administered with nontoxic dosages of EBB (IC(10)). In vivo, EBB can prolong the lifespan of mice with ascites H22 to more than three months. 64% of mice survived, while all animals in the control group died by the 18th day. When EBB (5 mg x kg(-1) x d(-1)) is jointly used with 5-FU (25 mg x ml(-1) x d(-1)), 73% of mice with ascites H22 survived, much higher than 27% in the 5-FU treated group. EBB can enhance the anti-hepatoma ability of 5-Fu treatment. EBB mechanism against hepatoma: P53 expression in the EBB treated group is substantially higher than that in the control group. EBB increased the translation of P53. As a calmodulin antagonist, EBB decreases amount of the CaM in hepatoma cells and blocked the hepatoma cell proliferation cycle at the G(2)M phase. Before the G(0)/G(1) phase, a diploid peak and apoptic cells in the treated groups were observed. CONCLUSIONS: The CaM antagonist, EBB, has a strong anti-hepatoma effect and enhances the effect of 5-FU, induces hepatoma cell to apoptosis, promotes the P53 protein expression and decreases the amount of CaM in the cytoplasm. All these results demonstrate that EBB is a new and potentially useful drug against hepatoma and should be researched further.

Anti-tumor effect of human endostatin mediated by retroviral gene transfer in nude mice

OBJECTIVE: To explore the inhibitory effect of human endostatin gene mediated by retroviral vector on the growth of human liver carcinoma. METHODS: A recombinant retroviral plasmid containing human endostatin gene and signal peptide was engineered and transferred into PA317 cells to produce retrovirus. Human liver carcinoma cells (SMMC7721) were infected with the above retrovirus to build a stable endostatin-transfected liver carcinoma cell line (SMMC-endo). The control liver carcinoma cell line (SMMC-pLncx) was developed in a similar way except that the plasmid was replaced by an empty retroviral vector. Immunohistochemistry and Western blot were used to test the expression and secretion of human endostatin. The biological activity of the expressed human endostatin was assessed by endothelial cell proliferation assay. The growth rates of SMMC-endo and control SMMC-pLncx cells in vivo and in vitro were also observed. RESULTS: The expression and secretion of human endostatin by endostatin-transfected SMMC-endo cells were confirmed by immunohistochemistry and Western blot. Compared with the control group, concentrated supernatant of SMMC-endo cells remarkably inhibited the proliferation of human umbilical vein endothelial cells by 48%, significantly higher than the inhibition by the control (10.2%; P

Inhibitory effect of Sumu(Lignum Sappan) plus Fuzi(Radix Aconiti Lateralis Praeparata) on a lung carcinoma model

OBJECTIVE: To investigate the inhibitory effect of Sumu(Lignum Sappan) plus Fuzi(Radix Aconiti Lateralis Praeparata)(SF) on the growth and metastasis of Lewis lung carcinoma.METHODS: A lung carcinoma model was established by subcutaneously inoculating Lewis lung carcinoma cells into C57 BL/6 mice. The mice were randomly divided into four groups of 13 mice(control, low-dose, moderate-dose, and high-dose), and gavaged once-daily for 21 consecutive days. The rates of tumor inhibition, metastasis, and metastasis inhibition were observed. The differential expressions of s P-selectin and vascular endothelial growth factor C(VEGFC) were compared between the treatment groups and the control group.RESULTS: The tumor weights differed significantly between the treatment groups and the control group(P < 0.05). Administration of SF in the moderate-dosage and low-dose groups significantly inhibited the expression of s P-selectin and VEGFC(both P < 0.05), suggesting anti-tumor activity.CONCLUSION: SF can inhibit the growth and metastasis of Lewis lung carcinoma.