Clinicopathological significance of platelet-derived growth factor B, platelet-derived growth factor receptor-β, and E-cadherin expression in gastric carcinoma.

Clinicopathological significance of platelet-derived growth factor B, platelet-derived growth factor receptor-β, and E-cadherin expression in gastric carcinoma.
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DOI:
10.5114/wo.2013.34618
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发表时间:
2013
期刊:
Contemporary oncology (Poznan, Poland)
影响因子:
--
通讯作者:
Wang Z
Wang Z
中科院分区:
其他
文献类型:
--
作者:
Guo Y;Yin J;Zha L;Wang Z

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血小板源性生长因子B (platelet derived growth factor B, PDGF-B)是一种重要的生长因子,可诱导血管生成和上皮间质转化(epithelial-mesenchymal transition, EMT),在许多肿瘤的转移中起重要作用。然而,PDGF-B在胃癌中的作用在很大程度上是未知的。我们通过研究PDGF-B、PDGFR-β和E-cadherin的表达与胃癌患者临床特征的相关性,探讨PDGF-B信号通路、E-cadherin与胃癌转移的关系,以及PDGF-B信号通路与E-cadherin表达的相关性,探讨PDGF-B信号通路在胃癌转移中的作用。我们检测64例手术切除的胃癌患者胃癌组织和正常胃粘膜组织中PDGF-B、PDGFR-β和E-cadherin的表达,探讨其与临床特征的关系以及PDGF-B和E-cadherin在胃癌组织中的表达关系。在手术标本中,肿瘤细胞表达PDGF-B,肿瘤基质细胞表达PDGFR-β。肿瘤细胞和正常胃粘膜细胞均表达E-cadherin。胃癌组织中PDGF-B、PDGFR-β表达升高(p < 0.05),并与肿瘤浸润深度、淋巴结转移及TNM分期呈正相关(p < 0.05)。E-cadherin在胃癌组织中表达降低(p < 0.05),并与癌浸润深度、淋巴结转移及TNM分期呈负相关(p < 0.05)。PDGF-B与E-cadherin表达呈负相关(p < 0.05)。我们的数据表明,PDGF-B和PDGFR-β的过表达或E-cadherin的过表达与胃癌的进展和淋巴转移有关。PDGF-B信号通路可能通过下调E-cadherin的表达诱导EMT,促进胃癌转移。
Platelet-derived growth factor B (PDGF-B), a vital growth factor which can induce angiogenesis and epithelial-mesenchymal transition (EMT), is important in the metastasis of many tumors. However, the roles of PDGF-B in gastric carcinoma are largely unknown. We investigated the correlation between PDGF-B, PDGFR-β and E-cadherin expression with the clinical features of gastric carcinoma patients to evaluate the relationship between PDGF-B signaling, E-cadherin and metastasis of gastric carcinoma, the correlation between PDGF-B and E-cadherin expression to assess the roles of PDGF-B signaling in metastasis of gastric carcinoma.. We detected expressions of PDGF-B, PDGFR-β and E-cadherin in gastric carcinoma tissues and normal gastric mucosa tissues of 64 patients with gastric carcinoma who had undergone surgical resection, and investigated their relationships with clinical features and the relationships between PDGF-B and E-cadherin expression in gastric carcinoma. In surgical specimens, tumor cells expressed PDGF-B, and PDGFR-β was expressed by tumor stromal cells. E-cadherin was expressed by both tumor cells and normal gastric mucosa cells. Expressions of PDGF-B and PDGFR-β were increased in gastric carcinoma tissues (p < 0.05) and were positively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The expression of E-cadherin was reduced in gastric carcinoma tissues (p < 0.05) and was negatively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The correlation between PDGF-B and E-cadherin expression was negative (p < 0.05). Our data indicate that either the overexpression of PDGF-B and PDGFR-β or the underexpression of E-cadherin is correlated with cancer progression and lymphogenous metastasis of gastric carcinoma. The PDGF-B signal pathway might induce EMT by down-regulating expression of E-cadherin to promote metastasis of gastric carcinoma.