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Objective To investigate the effect of recombinant human endostatin (Endostar) combined with hepatic artery interventional therapy on the progression-free survival (PFS) of patients with advanced hepatocellular carcinoma (HCC). MethodsA total of 86 patients with advanced HCC who were admitted to Fujian Provincial Tumor Hospital from March 2011 to May 2015 were selected and divided into treatment group and control group according to a matched pair design. The treatment group (43 patients) was given Endostar combined with hepatic artery interventional therapy, and the control group (43 patients) was given hepatic artery interventional therapy combined with oral administration of Ganfule. The chi-square test was applied for comparison of categorical data between the two groups, and the t-test was applied for comparison of continuous data between the two groups. The Kaplan-Meier method was applied for survival analysis, the Log-rank test was applied for univariate analysis, and Cox proportional hazards model was applied for multivariate analysis. ResultsThe median PFS in the treatment group and the control group was 154 d ［95% confidence interval (CI): 94-214 d］ and 70 d (95%CI: 39-101 d), respectively, with a significant difference between the two groups (χ2=10.741, P=0.001). Univariate analysis showed that the severity of liver cirrhosis, number of tumors, and main portal vein tumor thrombus/inferior vena cava tumor thrombus were the prognostic factors for patients with advanced HCC (χ2=8.182, 9.150, and 6.565, P=0.004, 0.027, and 0.038); multivariate analysis showed that the severity of liver cirrhosis and main portal vein tumor thrombus/inferior vena cava tumor thrombus were the independent prognostic factors for PFS in patients with advanced HCC who were treated with Endostar combined with hepatic artery interventional therapy (P=0.028 and 0.013). ConclusionEndostar can effectively prolong the PFS of patients with advanced HCC after hepatic artery interventional therapy, but it does not have a clear advantage in patients with severe liver cirrhosis or main portal vein tumor thrombus/inferior vena cava tumor thrombus. [ABSTRACT FROM AUTHOR]

Objective: To study the effects of murine angiostatin, which was transfected into the human hepatocellular cancer cell line SMMC-7721, on the implant carcinoma of nude mouse., Methods: The human hepatocellular cancer cell line SMMC-7721, which could express murine angiostatin gene stably, was constructed. The animals were divided into three groups: SMMC-7721 cell was implanted into control group, SMMC-7721/pcDNA3.1 (+) cell was implanted into vector group, and SMMC-7721/pcDNA3.1-mAST cell was implanted into angiostatin group. The carcinoma volume, weight, and microvessel density (MVD) of each group were compared., Results: The implant carcinoma volume in 35 days was (3 538.1 +/- 643.3) mm(3), (3 128.5 +/- 546.6) mm(3), and (755.8 +/- 198.2) mm(3) in the control group, vector group, and angiostatin group. The carcinoma weight of the control group, vector group, and angiostatin group was (6.0 +/- 0.7) g, (5.9 +/- 0.5) g, (2.1 +/- 0.5) g, respectively. The carcinoma MVD was 52.2 +/- 6.6, 49.4 +/- 7.0, and 25.5 +/- 4.1 accordingly. The carcinoma volume, weight, and MVD of the angiostatin group were significantly smaller than those of the control group and vector group (P < 0.01). The inhibitory rate of carcinoma reached 78.6%., Conclusions: Nude mouse experiments showed that the tumorigenic capacity of cells transfected had been reduced greatly, and that the carcinoma volume, weight and MVD were significantly lower than those of the control group. We conclude that angiostatin inhibits the growth of carcinoma by its inhibition of carcinoma angiogenesis.

Objective: To discuss the feasibility of human glioma therapy by the local secretion of angiostatin K(1-3)[AK(1-3)]., Method: AK(1-3) cDNA with secretive signal was inserted into polylinker sites of eukaryotic expression vector pcDNA3 to construct pcDNA-SAK(1-3); The vector was transfected into human glioma SHG44 cells by lipofectamine and the positive clone was screened by G418. The biological characters of glioma cells were examined with electron microscopy and FCM. The activity of AK(1-3) protein expressed by the SHG44 cells was examined by the endotheliocyte inhibition assay and immunofluorescence assay. When the tumor cells were implanted into nude mice, the tumor necrosis and micrangium was calculated by immunohistochemistry and electron microscopy in order to determine the influence of AK(1-3) protein to the human glioma growth., Results: The pcDNA-SAK(1-3) vector was successfully constructed and transfected into glioma cells that could express AK(1-3) protein. The tumorigenesis and angiogenesis of glioma cells in nude mice were greatly reduced (tumour end volume, experiment group 170 mm3, control group 8 120 mm3, P < 0.01; Blood vessel counting, experimental group 5.4, control group 12.2, P < 0.01)., Conclusion: The human glioma angiogenesis and growth were inhibited by the local secretion of AK(1-3). It can be further used in the treatment of other solid tumors.

Objective: To study the antitumor effect of angiostatin on LA795 adenocarcinoma cells inoculated on T739 mice., Methods: Affinity chromatography purified plasminogen was digested by pancreatic elastase and angiostatin was obtained by purifying the digestion with affinity chromatography and dialysis. T739 mice were inoculated with LA795 cells. Angiostatin was given to part of inoculated and uninoculated mice by intraperitoneal injection fourteen days after the inoculation. The treatment lasted 20 days and the size of tumor, survival period, behavior of the mice and pathology of lungs, livers and kidneys were observed., Results: The size of tumor decreased from (2.35 +/- 0.26) cm to (0.97 +/- 0.34) cm after angiostatin treatment. The number of metastases in lung was significantly fewer in angiostatin treated mice than in untreated ones, which lived much shorter. No obvious side effects were observed., Conclusion: Angiostatin markedly inhibits the growth and metastasis of LA795 cells on T739 mice and no obvious side effects of angiostatin were found during the treatment.