PRL-3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma.
PRL-3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma.
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DOI：
10.1111/jop.12331
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发表时间：
2016-02
期刊：
影响因子：
--
通讯作者：
Wang A
中科院分区：
文献类型：
--
作者：
Dong Q;Ding X;Chang B;Wang H;Wang A
PRL-3已被发现与多种恶性肿瘤的发生有关。在这项研究中，我们研究了PRL-3在涎腺腺样囊性癌(SACC)的发生、转移和侵袭中的作用。免疫组织化学(IHC)分析PRL-3在SACC发生、发展及预后中的作用。然后，我们在配对的SACC细胞中过表达或抑制PRL-3的表达，以分析PRL-3在SACC迁移和侵袭中的作用。采用体外迁移和侵袭实验。Western blotting检测转移相关蛋白水平。IHC结果证实，PRL-3的表达下调是SACC的常见事件；PRL-3的表达上调与临床分期、生命状态和远处转移有关，与总体生存率和无瘤生存率降低有关。具有较高迁移和侵袭能力的SACC-LM细胞比具有较低迁移和侵袭能力的SACC-83细胞具有更强的PRL-3蛋白表达。在SACC-83细胞中，PRL-3过表达促进细胞迁移、侵袭和增殖，同时导致磷酸化PRL-3、pERK1/2、slug、Vimentin表达上调，E-cadherin表达下调。然而，在SACC-LM细胞中，PRL-3抑制剂或PRL-3 siRNA抑制细胞的迁移、侵袭和增殖，导致磷酸化的PRL-3、pERK1/2、slug、Vimentin的下调和E-cadherin的上调。我们的结果证实了PRL-3在SACC的发生发展中起重要作用，并有助于SACC的迁移和侵袭能力。
PRL‐3 had been found to be involved in tumorigenesis in various malignancies. In this study, we investigated the role of PRL‐3 in the development, migration, and invasion of salivary adenoid cystic carcinoma (SACC). Immunohistochemistry (IHC) was used to analyze the role of PRL‐3 in the development and prognosis of SACC. Then, we overexpressed or inhibited the expression of PRL‐3 in paired SACC cells to analyze the role of PRL‐3 in the migration and invasion of SACC. In vitro migration and invasion assays were used. Western blotting was used to detect metastasis‐related protein levels. IHC results confirmed that the deregulation of PRL‐3 was a frequent event in SACC; the upregulation of PRL‐3 was related to clinical stages, vital status, and distant metastasis, which was associated with reduced overall survival and disease‐free survival. SACC‐LM cells with higher migratory and invasive abilities had more robust PRL‐3 protein expression than SACC‐83 cells with lower migratory and invasive abilities. PRL‐3 overexpression promoted cell migration, invasion, and proliferation, led to simultaneous upregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and downregulation of E‐cadherin in SACC‐83 cells. However, the inhibition of PRL‐3 by PRL‐3 inhibitor or PRL‐3 siRNA in SACC‐LM cells inhibited cell migration, invasion, and proliferation, resulted in simultaneous downregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and upregulation of E‐cadherin. Our results confirm that PRL‐3 plays an important role in the development of SACC and contributes to the migratory and invasive abilities of SACC.
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