Abstract
To investigate the effects of endostar, a recombined humanized endostatin, plus cisplatin on the growth, lymphangiogenesis and lymphatic metastasis of the Lewis lung carcinoma (LLC) in mice. A tumor model were established in C57BL/6 mice by intravenious transplantation of LLC cells. Then the mice were randomized to receive administration with NS, endostar, cisplatin, or endostar plus cisplatin. After the mice were sacrificed, tumor multiplicity, tumor size and lymph node metastasis were assessed. Then the expression of vascular endothelial growth factor-c (VEGF-C) and podoplanin were determined by immunohistochemical staining. Endostar plus cisplatin significantly suppressed tumor growth. lymphatic metastasis and prolonged survival time of the mice without obvious toxicity. The inhibition of lymphatic metastasis was associated with decreased microlymphatic vessel density (MLVD) and expression of VEGF-C. Endostar combined with cisplatin was more effective to suppress tumor growth and lymphatic metastasis than either agent alone. Thus this may provide a rational alternative for lung carcinoma treatment.
Highlights
Chemotherapy is the leading treatment for malignant tumor, and cisplatin has been administered frequently for lung cancer
Treatment with endostar or cisplatin as the single agent resulted in significant regression of tumor growth and prolonged survival time compared with the NS groups (P
Chemotherapy is often followed by serious mice treated with NS or cisplatin, showed larger microlymphatic vessel density (MLVD) side effects such as nausea, vomiting, neurotoxicity and than the other two groups (P
Summary
Chemotherapy is the leading treatment for malignant tumor, and cisplatin has been administered frequently for lung cancer. Chemotherapy for malignant tumors is still insufficien, and lymphatic metastasis is a major prognostic factor in lung carcinoma. An approach combining chemotherapy with antiangiogenesis factors has been reported in treatment for established animal tumors (Huang et al, 2010). Endostatin is a internal fragment of the carboxyterminus of collagen XVIII, first produced by hemangioendothelioma (O’Reilly et al, 1997), capable of inhibiting endothelial cell proliferation and inducing endothelial cell apoptosis, which has been reported as one of the most potent endothelial cell inhibitors of angiogenesis and tumor growth (Boehm et al, 1997). Studies have showed that endostar can improve the response rate and progression-free survival when used in combination with chemotherapy regime in patients with advanced non-small-cell lung cancer (Sun et al, 2005; Rong et al, 2012)
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