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首页> 外文期刊>Cytokine >VEGF-C promotes the development of esophageal cancer via regulating CNTN-1 expression.
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VEGF-C promotes the development of esophageal cancer via regulating CNTN-1 expression.

机译：VEGF-C通过调节CNTN-1表达促进食道癌的发展。

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Vascular endothelial growth factor C (VEGF-C) is a key regulator of angiogenesis and lymphangiogenesis. VEGF-C is also implicated in the development of esophageal cancer. We investigated the mRNA levels of VEGF-C and its receptors in 38 esophageal squamous cell carcinoma specimens (ESCCs) and matched adjacent normal esophageal tissues via real-time PCR. The mRNA levels of VEGF-C, VEGFR-2 and VEGFR-3 were significantly upregulated in ESCCs versus respective side normal tissues. To explore the influence of VEGF-C on esophageal cancer progression, the expression of VEGF-C was manipulated in esophageal cancer cell lines TE-1 and Eca-109. VEGF-C transcription, translation and secretion were significantly enhanced in cells stably transfected with a VEGF-C overexpression vector or attenuated in VEGF-C shRNA-transfected cell lines. In vitro, TE-1 cells stably transfected with a VEGF-C overexpression vector exhibited an increased rate of cell proliferation, migration and focus formation, whereas knockdown of VEGF-C inhibited cell proliferation, migration and focus formation. Similar results were obtained for Eca-109 cells. VEGF-C mediated biological function through transcription of CNTN-1, which is implicated in tumor invasion and metastasis. The expression of VEGF-C was correlated with that of CNTN-1 and cell proliferation and migration induced by VEGF-C were reversed by silencing of CNTN-1. In addition, nude mice inoculated with VEGF-C shRNA-transfected cells exhibited a significantly decreased tumor size in vivo via reduced VEGFR-2 and VEGFR-3 phosphorylation and microvessel formation. VEGF-C upregulation may be involved in esophageal tumor progression. Vector-based RNA interference (RNAi) targeting VEGF-C is a potential therapeutic method for human esophageal carcinoma.
机译：血管内皮生长因子C（VEGF-C）是血管生成和淋巴管生成的关键调节剂。 VEGF-C也与食道癌的发生有关。我们通过实时PCR研究了38例食管鳞状细胞癌标本（ESCC）和匹配的邻近正常食管组织中VEGF-C及其受体的mRNA水平。与各个侧面正常组织相比，ESCC中VEGF-C，VEGFR-2和VEGFR-3的mRNA水平显着上调。为了探讨VEGF-C对食管癌进展的影响，在食管癌细胞系TE-1和Eca-109中操纵了VEGF-C的表达。在用VEGF-C过表达载体稳定转染的细胞中或在VEGF-C shRNA转染的细胞系中减毒的细胞中，VEGF-C的转录，翻译和分泌显着增强。在体外，用VEGF-C过表达载体稳定转染的TE-1细胞表现出增加的细胞增殖，迁移和焦点形成速率，而敲低VEGF-C抑制细胞增殖，迁移和焦点形成。 Eca-109细胞获得了相似的结果。 VEGF-C通过CNTN-1的转录介导生物学功能，这与肿瘤的侵袭和转移有关。 VEGF-C的表达与CNTN-1相关，而沉默CNTN-1可逆转VEGF-C诱导的细胞增殖和迁移。另外，用VEGF-C shRNA转染的细胞接种的裸鼠通过减少的VEGFR-2和VEGFR-3磷酸化和微血管形成，在体内表现出明显减小的肿瘤大小。 VEGF-C上调可能与食管肿瘤的进展有关。靶向VEGF-C的基于载体的RNA干扰（RNAi）是人类食管癌的潜在治疗方法。

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