CD200-CD200R affects cisplatin and paclitaxel sensitivity by regulating cathepsin K-mediated p65 NF-κB signaling in cervical cancer

BackgroundCD200-CD200R plays a critical role in regulating the human tumor microenvironment, but its cervical cancer remains unclear.MethodsA total of 62 paraffin blocks tissues were collected from patients. Expression CD200 and cathepsin K (CTSK) para-cancerous was analyzed by immunohistochemistry. Stably transfected cells established HeLa SiHa cells. Human THP-1 monocytes induced to differentiate into M2 macrophages. cultured conditioned medium macrophages observe effects CD200-CD200R on invasion, CTSK, p65NF-κB, cisplatin or paclitaxel sensitivity injected induce xenograft tumors mice, CTSK inhibitor, MK-0822, used confirm regulation vivo.ResultsA significant decrease expression found compared with tissues. Only overexpression did not affect cell could enhance invasion resistance paclitaxel. Meanwhile, p-p65NF-κB stably obviously increased after culture transfection plasmid control. In vivo, inhibition significantly suppressed response suppressing CTSK-mediated NF-κB pathway.ConclusionsCD200-CD200R regulates pathway cancer, which provides possible immunotherapeutic target combination strategy for advanced cancer.