| http://purl.uniprot.org/citations/32167616 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32167616 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcla.23283"xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/author | "Zhao Y."xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/name | "J Clin Lab Anal"xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/pages | "e23283"xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/title | "Block of proliferation 1 promotes cell migration and invasion in human colorectal cancer cells via the JNK pathway."xsd:string |
| http://purl.uniprot.org/citations/32167616 | http://purl.uniprot.org/core/volume | "34"xsd:string |
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