B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer
B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer
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DOI：
10.3892/mmr.2015.4050
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发表时间：
2015-10-01
影响因子：
3.4
通讯作者：
Hua, Dung
中科院分区：
文献类型：
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作者：
Liu, Fen;Zhang, Ting;Hua, Dung
B7-H3是一种新发现的共刺激分子，已被报道在许多类型的癌症中高表达，并与不良预后有关。通过Transwell实验和伤口愈合实验检测过表达的B7-H3对结直肠癌(CRC)细胞迁移和侵袭的作用。通过酶谱实验和Western印迹分析进一步检测基质金属肽酶9(MMP9)的表达水平，并用JAK2选择性抑制剂AG490检测JAK2信号转导和转录激活因子3(STAT3)信号通路的参与情况。资料显示，B7-H3过表达促进了结直肠癌细胞的迁移和侵袭。进一步的研究证实，B7-H3的增强表达通过上调JAK2-STAT3信号通路上调了基质金属蛋白酶-9。由于它的.B7-H3具有亲迁移和亲侵袭的功能，可作为治疗结直肠癌的靶点。
B7-H3, a newly identified co-stimulatory molecule, has been reported to be highly expressed in a number of types of cancer and is associated with a poor prognosis. Transwell experiments and a wound-healing assay were used to detect the role of over-expressed B7-H3 on cell migration and invasion in colorectal cancer (CRC) cells. The expression level of matrix metallopeptidase 9 (MMP-9) was further investigated by zymography experiments and western blot analysis, and involvement of the Janus kinase 2 (Jak2) signal transducer and activator of transcription 3 (STAT3) signaling pathway was determined using AG490, a Jak2 selective inhibitor. Data showed that overexpression of B7-H3 promoted cell migration and invasion in CRC. Further investigation certified that enhanced expression of B7-H3 elevated MMP-9 through upregulation of the Jak2-Stat3 signaling pathway. Due to its. pro-migratory and pro-invasive function, B7-H3 may serve as a therapeutic target in the treatment of CRC.