Endostatin gene therapy enhances the efficacy of paclitaxel to suppress breast cancers and metastases in mice

Li, Jie; Dong, Xuesong; Xu, Zuowei; Jiang, Xian; Jiang, Hongchi; Krissansen, Geoffrey W.; Sun, Xueying

doi:10.1007/s11373-007-9201-3

Cited by 15 publications

(14 citation statements)

References 56 publications

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“…The expression of endostatin detected by RT-PCR and western blot analysis was low and the tumor inhibitory effect was not significant. Although a number of studies reported that endostatin treatment reduced tumor growth rates and induced the regression of established tumors (2,(29)(30)(31), complete tumor inhibition was not readily achieved.…”

Section: Discussionmentioning

confidence: 99%

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Effects of the C-terminal of endostatin on the tumorigenic potential of H22 cells

Liu

Wei

et al. 2013

Biomedical Reports

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Abstract.Endostatin is an endogenous angiogenesis inhibitor whose specific functional site has not yet been determined. In the present experiment, 13 amino acids (LCIENSFMTSFSK) were selectively deleted from the C-terminal of endostatin and the resulting mutant endostatin was named EM13. To determine the effect of the C-terminal deletion on the biological activity of endostatin, EM13, wild-type endostatin and empty plasmid were transfected into H22 cells. After 48 h, the three types of transfected cells were harvested and injected into nude mice. The results demonstrated that there was no significant difference in tumor size, as determined by hematoxylin and eosin staining, between the EM13-transfected group and the endostatin and empty plasmid groups, although the nude mice that were injected with EM13-transfected H22 cells exhibited smaller tumors and lower density of blood vessels compared to those injected with endostatin-and empty plasmid-transfected H22 cells. The results suggested that the 13 amino acids of the C-terminal of endostatin do not play an important role in the tumorigenic potential of H22 cells. This experiment was unsuccessful in reproducing the results of several investigators. Therefore, the mechanism underlying the tumorigenesis of H22 cells remains to be elucidated.

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Section: Discussionmentioning

confidence: 99%

“…Endostatin is one of the most potent inhibitors of angiogenesis and may induce tumor regression in mice (1,2). Clinical trials on the antitumor effects of endostatin are currently ongoing (3).…”

Section: Introductionmentioning

confidence: 99%

Effects of the C-terminal of endostatin on the tumorigenic potential of H22 cells

Liu

Wei

et al. 2013

Biomedical Reports

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“…The lungs and liver were harvested and the surface nodules were counted to evaluate the metastatic spread of the tumor. The tissues were fixed in 4% paraformaldehyde and stained with hematoxylin and eosin (20,21).…”

Section: Assessment Of Tumor Volume and Metastasis The Tumor Volume mentioning

confidence: 99%

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

et al. 2011

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Abstract. Vascular endothelial growth factor-A (VEGF-A)affects tumor growth and metastasis through stimulation of angiogenesis. The purpose of this study was to describe features of Lewis lung cancer (LLC) in mice and compare the serum VEGF-A levels with those of normal control mice. Two groups of mice were compared: one was subcutaneously injected with LLC cells (n=16) and the other served as the normal control (n=6). The serum VEGF-A levels were measured by ELISA prior to inoculation, and at 7, 21 and 35 days post-inoculation. The tumor weight and the metastatic condition were evaluated on day 35. Changes in body weight and serum VEGF-A concentration over a period of time were compared between the groups using generalized estimating equations. The relationship between the primary tumor and the metastatic condition was analyzed using the Spearman's rank correlation test. The survival rate was 56.3% on day 35 post-tumor inoculation. No difference was found between the groups with regard to gastrocnemius muscle weight on day 35 post-inoculation [0.1315±0.0066 g vs. 0.1308±0.0069 g (normal control)]. In tumor-bearing mice, the weight gain at sacrifice was less (0.24±0.45 vs. 1.93±0.47 g, P= 0.01), the final mean tumor volume and weight were 4264.69±1038.32 mm 3 and 3.70±0.83 g, the number of nodules in the lungs and livers was 6.33 (range 0-20) and 2.22 (range 0-11), respectively, and the serum VEGF-A levels were significantly higher than those of control mice. In conclusion, lower body weight gain, metastasis in the liver and lungs, and elevated VEGF-A levels are features of LLC in mice.

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“…This tumor shares many characteristics with human mammary cancers, it closely resembles stage IV human breast cancer, making it an excellent animal model. It was used to investigate inhibitors of DNA-binding proteins necessary for cancer stem cells [26], chemoresistance [27], antimetastatic activities of various drugs and drug combination [28,29]. 4T1/luc cells were engineered for stable expression of firefly luciferase to allow tracking and quantifying of the cells in vivo.…”

Section: Discussionmentioning

confidence: 99%

Lidamycin inhibits tumor growth and pulmonary metastasis in murine breast carcinoma and shows synergy with paclitaxel

Zhang

Shao

et al. 2013

Chin. Sci. Bull.

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The main goal of this study was to investigate whether lidamycin (LDM) could enhance the efficacy of paclitaxel (TAX) against breast cancer. In the MTT assay, LDM showed much more potent cytotoxicity than paclitaxel, and there was a synergy on the 4T1/luc breast cancer cells treated with a combination of paclitaxel and LDM. Western blot analysis showed that paclitaxel and LDM synergistically downregulated MMP9, MMP2, VEGF, and upregulated the cleaved PARP proteins. By wound closure cell migration assay, paclitaxel combined LDM obviously inhibited the migration of 4T1/luc cells. At therapeutic dosage level, LDM, paclitaxel, and the combination suppressed the pulmonary metastases by 70.2%, 53.8%, and 88.7%, respectively, and the CDI value was 0.82, indicating synergism. The results show that LDM enhances the antitumor effect of paclitaxel on 4T1/luc breast cancer, in particular, the antimetastatic effects on pulmonary metastasis. lidamycin, paclitaxel, breast cancer, antitumor, antimetastatic Citation:Hu L, Zhang S H, Shao R G, et al. Lidamycin inhibits tumor growth and pulmonary metastasis in murine breast carcinoma and shows synergy with paclitaxel.

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Endostatin gene therapy enhances the efficacy of paclitaxel to suppress breast cancers and metastases in mice

Cited by 15 publications

References 56 publications

Effects of the C-terminal of endostatin on the tumorigenic potential of H22 cells

Effects of the C-terminal of endostatin on the tumorigenic potential of H22 cells

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

Lidamycin inhibits tumor growth and pulmonary metastasis in murine breast carcinoma and shows synergy with paclitaxel

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