肺肉瘤样癌中血管生成拟态的形成及其与上皮间充质转化的关系

Relationship between vasculogenic mimicry and epithelial-to-mesenchymal transition in pulmonary sarcomatoid carcinoma

    摘要
  • 摘要:
      目的  研究肺肉瘤样癌(pulmonary sarcomatoid carcinoma, PSC)中血管生成拟态(vasculogenic mimicry, VM)的临床意义, 阐述上皮间充质转化(epithelial-to-mesenchymal transition, EMT)提高PSC的恶性度及促进VM形成的相关机制。
      方法  对肺肉瘤样癌组织切片22例进行HE、CD31和PAS双重染色, Twist、Vimentin、E-cadherin、VEGF免疫组织化学染色, 分析VM相关的临床意义及EMT促进VM形成的相关机制。
      结果  22例中4例(18.2%)存在VM, Kaplan-Meier生存分析提示有无VM肿瘤患者比较生存时间差异有统计学意义(P < 0.05)。VM阳性患者Twist的阳性率较阴性患者高, 且差异有统计学意义(P < 0.05)。Twist1的表达与VEGF、E-cadherin、Vimentin的表达存在明显相关性。
      结论  VM是患者预后的不利因素, 肺肉瘤样癌中发生了EMT, 转录因子Twist1可能通过下调E-cadherin, 上调Vimentin诱导EMT, 并可能通过上调VEGF的表达促进VM的形成, 从而促进肿瘤的侵袭和转移。

     

    Abstract:
      Objective  The expression and clinical significance of vasculogenic mimicry(VM) were investigated.The related mechanisms of epithelial-to-mesenchymal transition(EMT) in VM formation and worsening of pulmonary sarcomatoid carcinoma(PSC) were examined.
      Methods  Hematoxylin and eosin staining, CD31/periodic acid-Schiff double staining, and immunohistochemical staining were performed to determine the expression of VM, Twist1, vascular endothelial growth factor(VEGF), E-cadherin, and vimentin in the tissues of 22 PSC patients.The clinical significance of VM and the mechanism of EMT in VM formation were explored.
      Results  VM was found in four(18.2%) of the 22 PSC patients.Kaplan–Meier survival analysis revealed that the patients with VM had a shorter survival period than those without the VM expression, with statistically significant differences found between the two groups.Comparative results of the groups with and without VM expression showed a higher positive rate of Twist1 expression in the former group(P < 0.05).Significant correlations were observed between the Twist1 expression and the VEGF, E-cadherin, and vimentin expression.
      Conclusion  VM unfavorably influences the prognosis of PSC patients.Twist1 can upregulate Vimentin and downregulate E-cadherin by inducing EMT.Additionally, it may upregulate VEGF to promote VM formation, which increases tumor invasions and metastases.

     

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