Department of Gastroenterology, Affiliated Maternity and Child Health Care Hospital of Nantong University, Nantong, China.
Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao, China.
J Clin Lab Anal. 2020 Jul;34(7):e23283. doi: 10.1002/jcla.23283. Epub 2020 Mar 13.
Metastasis is one of the most common causes of death in patients with colorectal cancer (CRC). Block of proliferation 1 (BOP1) regulates tumorigenesis, epithelial-to-mesenchymal transition, migration, metastasis, and drug resistance in several tumor types. However, the role of BOP1 in the regulation of colorectal cancer cell migration and invasion is still largely unclear. In this study, the results of immunohistochemistry showed that BOP1 was upregulated in our cohort of CRC patients. BOP1 knockdown inhibited the migration and invasion of CRC cells, confirmed by the downregulation of the mRNA levels of MMP-2 and MMP-9. The overexpression of BOP1 in CRC cells exerted the opposite effect. SP600125, an inhibitor of JNK signaling, partially abolished the BOP1 overexpression-mediated increase in the migratory and invasive ability of CRC cells. Our results indicated that BOP1 is an important regulator of CRC cell invasion and migration, predominantly through the JNK signaling pathway.
转移是结直肠癌(CRC)患者死亡的最常见原因之一。增殖阻断蛋白 1(BOP1)在多种肿瘤类型中调节肿瘤发生、上皮间质转化、迁移、转移和耐药性。然而,BOP1 在调节结直肠癌细胞迁移和侵袭中的作用在很大程度上仍不清楚。在本研究中,免疫组织化学的结果表明,BOP1 在我们的 CRC 患者队列中上调。BOP1 敲低抑制了 CRC 细胞的迁移和侵袭,这通过 MMP-2 和 MMP-9 的 mRNA 水平下调得到证实。CRC 细胞中 BOP1 的过表达则产生了相反的效果。JNK 信号通路的抑制剂 SP600125 部分消除了 BOP1 过表达介导的 CRC 细胞迁移和侵袭能力的增加。我们的结果表明,BOP1 是 CRC 细胞侵袭和迁移的重要调节因子,主要通过 JNK 信号通路。