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B7-H3通过JAK2/STAT3信号通路调节涎腺腺样囊性癌的迁移和侵袭。

B7-H3 regulates migration and invasion in salivary gland adenoid cystic carcinoma via the JAK2/STAT3 signaling pathway.

作者信息

Fan Teng-Fei, Deng Wei-Wei, Bu Lin-Lin, Wu Tian-Fu, Zhang Wen-Feng, Sun Zhi-Jun

机构信息

The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University Wuhan, China.

The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan UniversityWuhan, China; Department of Oral Maxillofacial-Head Neck Oncology, School and Hospital of Stomatology, Wuhan UniversityWuhan, China.

出版信息

Am J Transl Res. 2017 Mar 15;9(3):1369-1380. eCollection 2017.

PMID:28386362
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5376027/
Abstract

B7 Homolog 3 (B7-H3), a newly identified member of the B7 family, is over-expressed in various human cancers and plays a vital role in tumor progression. To identify the expression pattern of B7-H3 in human salivary adenoid cystic carcinoma (AdCC) and its underlying mechanisms, we characterized B7-H3 expression in AdCC tissue microarrays using immunohistochemical staining, and analyzed potentially associated molecules. The results showed that B7-H3 was highly expressed in salivary AdCC, compared with normal salivary glands. Statistical analyses of immunohistochemical staining showed that B7-H3 was closely correlated with Slug and p-STAT3. Functional studies showed that knockdown of B7-H3 in AdCC cell lines using RNA interference did not influence cell growth and apoptosis, but decreased migration and invasion . Further mechanism studies suggested that B7-H3 influenced the migration and invasion of AdCC cells by regulating the epithelial-mesenchymal transition via JAK2/STAT3 pathway components. Collectively, these findings suggested that B7-H3 may be a potential therapeutic target for AdCC.

摘要

B7 同源物 3(B7-H3)是 B7 家族新发现的成员,在多种人类癌症中过度表达,并在肿瘤进展中起重要作用。为了确定 B7-H3 在人类涎腺腺样囊性癌(AdCC)中的表达模式及其潜在机制,我们使用免疫组织化学染色对 AdCC 组织芯片中的 B7-H3 表达进行了表征,并分析了潜在相关分子。结果显示,与正常涎腺相比,B7-H3 在涎腺 AdCC 中高表达。免疫组织化学染色的统计分析表明,B7-H3 与 Slug 和 p-STAT3 密切相关。功能研究表明,使用 RNA 干扰在 AdCC 细胞系中敲低 B7-H3 不影响细胞生长和凋亡,但会降低迁移和侵袭能力。进一步的机制研究表明,B7-H3 通过 JAK2/STAT3 信号通路成分调节上皮-间质转化,从而影响 AdCC 细胞的迁移和侵袭。总的来说,这些发现表明 B7-H3 可能是 AdCC 的潜在治疗靶点。

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PDGF-D/PDGFRβ promotes tongue squamous carcinoma cell (TSCC) progression via activating p38/AKT/ERK/EMT signal pathway.血小板衍生生长因子-D/血小板衍生生长因子受体β通过激活p38/AKT/ERK/上皮-间质转化信号通路促进舌鳞状细胞癌(TSCC)进展。
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