Aberrant Wnt-1/beta-catenin signaling and WIF-1 deficiency are important events which promote tumor cell invasion and metastasis in salivary gland adenoid cystic carcinoma.
Aberrant Wnt-1/beta-catenin signaling and WIF-1 deficiency are important events which promote tumor cell invasion and metastasis in salivary gland adenoid cystic carcinoma.
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Wnt-1/β-catenin信号传导异常和WIF-1缺陷是促进唾液腺腺样囊性癌肿瘤细胞侵袭和转移的重要事件。
DOI：
10.3233/bme-151520
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发表时间：
2015
影响因子：
1
通讯作者：
Qianming Chen
中科院分区：
文献类型：
--
作者：
Rui;Ning Geng;Yuqiao Zhou;Dunfang Zhang;Longjiang Li;Jing Li;N. Ji;Min Zhou;Yu Chen;Qianming Chen
本研究探讨 Wnt 成分是否在癌变或唾液腺（也称为腺样囊性癌 (sAdCC)）的侵袭和转移中发挥作用。检查了几种具有低侵袭潜力 (ACC-2)、高转移潜力 (ACC-M) 和较高侵袭潜力 (T-ACC-M) 的 sAdCC 细胞系，以确定 Wnt 成分是否与肿瘤的侵袭和转移行为相关。免疫组织化学在 sAdCC 组织阵列中进行。与 ACC-2 相比，ACC-M 表达更高水平的 Wnt-1、β-catenin 和更低水平的 WIF-1（P<0.05）。与 ACC-2 和 ACC-M 相比，T-ACC-M 表现出 Wnt-1 和 β-连环蛋白 mRNA 增加，并减少 WIF-1。免疫组织化学显示，与正常唾液腺相比，sAdCC 中 Wnt-1 上调，WIF-1 下调。 β-连环蛋白存在于 sAdCC 的细胞质和细胞核中。观察到 sAdCC 中 E-钙粘蛋白的错位。这些结果表明 sAdCC 表现出 Wnt 成分的多种表达。它与这些细胞的侵袭表型有重要关系。
This study investigates whether Wnt components play a role in carcinogenesis, or the invasion and metastasis of salivary glands, also referred to as adenoid cystic carcinoma (sAdCC). Several sAdCC cell lines with low invasive potential (ACC-2), high metastatic potential (ACC-M), and higher invasive potential (T-ACC-M) were examined to determine whether Wnt components correlate with tumors' invasive and metastatic behavior. Immunohistochemistry was performed in a sAdCC tissue array. ACC-M expressed higher levels of Wnt-1, beta-catenin and lower WIF-1 compared to ACC-2 (P<0.05). T-ACC-M exhibited increased mRNA of Wnt-1 and beta-catenin, and decreased WIF-1 compared to ACC-2 and ACC-M. Immuno-histochemistry showed up-regulation of Wnt-1 and down-regulation of WIF-1 in sAdCC compared with normal salivary glands. Beta-catenin was found in the cytoplasm and nuclei of sAdCC. Dislocation of E-cadherin in sAdCC was observed. These results suggest that sAdCC exhibits diverse expressions of Wnt components. It has an important relationship with the invasive phenotype of these cells.
影响因子：
3.2
作者：
Takigawa Y;Brown AM
通讯作者：
Brown AM