S100A4 regulates E-cadherin expression in oral squamous cell carcinoma

S100A4 regulates E-cadherin expression in oral squamous cell carcinoma
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DOI:
10.1016/j.canlet.2004.12.046
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发表时间:
2005-12-18
期刊:
影响因子:
9.7
通讯作者:
Sasaki, T
Sasaki, T
中科院分区:
医学1区
文献类型:
--
作者:
Moriyama-Kita, M;Endo, Y;Sasaki, T

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S100A4在细胞周期进程和细胞运动中具有多种功能,并与癌症侵袭有关。本研究检测了S100A4、E-cadherin及其相关蛋白在不同侵袭表型、4C级和4D级口腔鳞状细胞癌(SCC)细胞系中的表达。用S100A4表达载体转染表达E-cadherin的4C级OSC-19细胞,检测稳定克隆中E-cadherin相关蛋白的表达,以阐明S100A4与E-cadherin的关系。S100A4在稳定转化的OSC-19 (OSC-19/S100A4)细胞中组成性过表达导致E-cadherin和β -catenin的下调。此外,表达S100A4 mRNA的4D级侵袭细胞系(HOC313和TSU)不表达E-cadherin、P-cadherin和β -catenin,而γ -catenin蛋白仅弱表达。因此,E-cadherin mRNA的表达与口腔SCCs中S100A4的表达呈负相关。有趣的是,血管内皮生长因子c在OSC-19/S100A4细胞中表达上调。综上所述,s100a4介导的E-cadherin表达调控可能在口腔SCC侵袭转移过程中发挥重要作用。2005爱思唯尔爱尔兰有限公司版权所有。
S100A4 has multiple functions in cell cycle progression and cell motility, and has been implicated in cancer invasion. In this study, we examined the expression of S100A4, E-cadherin and its related proteins in oral squamous cell carcinoma (SCC) cell lines with different invasive phenotypes, grade 4C and 4D. Furthermore, grade 4C OSC-19 cells expressing E-cadherin were transfected with S100A4-expression vector and the expression of E-cadherin-related proteins in the stable clone was examined to elucidate the relationship between S100A4 and E-cadherin. Constitutive over-expression of S100A4 in stable transformant of OSC-19 (OSC-19/S100A4) cells led to down-regulation of E-cadherin and beta-catenin. Furthermore, grade 4D invasive cell lines (HOC313 and TSU) expressing S100A4 mRNA did not express E-cadherin, P-cadherin, and beta-catenin, while gamma-catenin protein was only weakly expressed. Thus, the mRNA expression of E-cadherin was reversely correlated with S100A4 expression in oral SCCs. Interestingly, vascular endothelial growth factor-C was up-regulated in OSC-19/S100A4 cells. In summary, S100A4-mediated regulation of E-cadherin expression may play an important mechanism in invasion and metastasis of oral SCC. (c) 2005 Elsevier Ireland Ltd. All rights reserved.