B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer

Abstract

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.