Endostar, a modified endostatin inhibits non small cell lung cancer cell in vitro invasion through osteopontin-related mechanism

Ni, Qinggui; Ji, Hui; Zhao, Zhihui; Fan, Xin; Xu, Chengyun

doi:10.1016/j.ejphar.2009.04.032

Cited by 28 publications

(29 citation statements)

References 27 publications

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“…Investigators have previously reported that endostatin exerts antiangiogenic effects by blocking vascular endothelial growth factor (VEGF)-induced tyrosine phosphorylation of KDR/Flk-1 of endothelial cells (21). Dong et al (22) and Brideau et al (23) found that endostatin inhibits lymphangiogenesis by downregulating the tumor expression of VEGF-C. By contrast, the osteopontin-related mechanism may be mediated in endostatin antitumor activity (24). These data indicate that endostatin remains to be adequately elucidated.…”

Section: Discussionmentioning

confidence: 83%

Clinical significance of serum and tumor tissue endostatin evaluation in operable non-small cell lung cancer

Zhang

et al. 2014

Biomedical Reports

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Abstract. Endostatin, as the most potential antiangiogenic factor, is a naturally occurring fragment of collagen XVIII in bloodstream capable of inhibiting tumor growth and metastasis. This study was conducted to explore the clinical value of endostatin in serum and tumor tissue in patients with operable non-small cell lung cancer (NSCLC). ELISA and immunohistochemistry were applied to detect the expression of endostatin in serum and tumor tissue in 105 patient-matched operable NSCLC patients. The serum level of endostatin was significantly higher in NSCLC patients than healthy individuals (P=0.0018). Cases with poorer differentiation showed a higher endostatin serum level (P=0.008). There was no significant correlation between tumor tissue expression and clinical parameters, such as TNM stage, differentiation degree, histological type and lymph node invasion status. A stronger expression of endostain in tumor tissue was associated with a higher serum level (r=0.223). The univariate and multivariate analyses with Cox proportional hazards model for overall survival showed that tumor stage and node status were independent prognostic factors, whereas neither endostatin levels in serum nor in tumor tissue showed potential in predicting the long-term survival of operable NSCLC patients. In conclusion, the results observed in the present study did not support the prediction of overall survival in operable NSCLC based on the expression levels of endostatin in serum and tumor tissue.

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Section: Discussionmentioning

confidence: 83%

Clinical significance of serum and tumor tissue endostatin evaluation in operable non-small cell lung cancer

Zhang

et al. 2014

Biomedical Reports

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“…Lu et al [20] found that Endostar suppressed the adhesion of human breast cancer cell to the fibronectincoated substrate, inhibited the invasion of cells through reconstituted ECM and the expressions of MMP-2 and MMP-9. Ni et al [21] showed that osteopontin induced the expression and activation of pro-matrix metalloproteinase (MMP)-2, and pro MMP-9 secreted from non-small-cell lung cancer cells were blocked with Endostar treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Endostar was approved by the State Food and Drug Administration of China (SFDA) in 2005 for the treatment of non-small-cell lung cancer [20]. Several studies have provided evidence that Endostar can inhibit the growth of solid tumors including cancer of the breast, lung, stomach, bladder, colon/rectum, and pancreas both in vivo and in vitro [20][21][22][23][24][25][26][27]. As an inhibitor of angiogenesis, Endostar presents a promising therapeutic modality to treat cancer.…”

Section: Introductionmentioning

confidence: 99%

The inhibition of Endostar on the angiogenesis and growth of gastrointestinal stromal tumor xenograft

et al. 2011

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To investigate whether Endostar can inhibit the angiogenesis and growth of gastrointestinal stromal tumor (GIST) xenografts in nude mice and the feasibility of antiangiogenesis as a treatment modality for GIST. Twenty Balb/c-nu/nu mice burdened with GIST were randomly divided into two groups. Endostar (2 mg/kg) was injected around the tumor once per day for 10 days in the experimental group and with normal saline (NS) (0.1 ml) in the control group. The tumor bulk was measured every 5 days until 5 days after the end of the injections. The inhibition tumor rate (ITR) was calculated. Tumor bulk, microvascular density (MVD), rate of bcl-2-positive expression, and AI were assessed in the two groups. Tumor volumes were compared before and after treatment in the experimental group. The difference in tumor bulk between the two groups was not statistically significant before treatment (P = 0.628), but at the end of test, the difference was significant (P < 0.0001), and in the test group, the tumor bulk was also decreased significantly after treatment (P < 0.0001). The ITR was 86.5%. All xenografts showed CD117-positive staining. MVD and bcl-2-positive rate were lower in the experimental group than in the control group (P = 0.020 and P = 0.023, respectively). AI increased significantly in the experimental group compared with the control group (P = 0.020). Endostar can reduce angiogenesis,promote cell apoptosis, and inhibit the growth of a GIST xenograft. It is possible that Endostar will be used as an effective drug for GIST in the future.

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“…Such binding might be essential for vascular endothelial cells to adhere to and migrate onto basement membrane, and later to generate vascular structure. With regard to endostatin (collagen XVIII), effected as an ECMderived angiogenesis inhibitor and extensively used in the researches of pulmonary cancer [24,25], the inhibition effect of rhEDI-8t on the proliferation of vascular endothelial cells may be realized via cell surface receptors/proteins. RhEDI-8t or endostatin suppresses subretinal NV in rho/VEGF transgenic mice Rho/VEGF mice were treated with 1 μl (1 μg/μl) rhEDI-8t 1 (b, whole retina, arrows, n=13, each retina is n=1; d, magnified views of part of b, arrows) or endostatin (h, whole retina, arrows, n=10; j, magnified views of part of h, arrows) as positive control in one eye and vehicle in the fellow eye (a, g, whole retina, arrows; c, i, magnified views of part of a and g, arrows) by intravitreous injection atP14, perfused with fluorescein-labeled dextran at P21.…”

Section: Discussionmentioning

confidence: 99%

A potential therapeutic strategy for inhibition of ocular neovascularization with a new endogenous protein: rhEDI-8t

Zhang

Shen

Lü

et al. 2011

Graefes Arch Clin Exp Ophthalmol

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Endostar, a modified endostatin inhibits non small cell lung cancer cell in vitro invasion through osteopontin-related mechanism

Cited by 28 publications

References 27 publications

Clinical significance of serum and tumor tissue endostatin evaluation in operable non-small cell lung cancer

Clinical significance of serum and tumor tissue endostatin evaluation in operable non-small cell lung cancer

The inhibition of Endostar on the angiogenesis and growth of gastrointestinal stromal tumor xenograft

A potential therapeutic strategy for inhibition of ocular neovascularization with a new endogenous protein: rhEDI-8t

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