Title : Long-term use of indomethacin leads to poor prognoses through promoting the expression of PD-1 and PD-L2 via TRIF/NF-κB pathway and JAK/STAT3 pathway to inhibit TNF-α and IFN-γ in hepatocellular carcinoma.

Pub. Date : 2015 Sep 10

PMID : 26162855






5 Functional Relationships(s)
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1 Long-term use of indomethacin leads to poor prognoses through promoting the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway to inhibit TNF-alpha and IFN-gamma in hepatocellular carcinoma. Indomethacin programmed cell death 1 Mus musculus
2 Furthermore, long-term use of indomethacin increased the expression of PD-1 and PD-L2 in programmed death-1 pathway. Indomethacin programmed cell death 1 Mus musculus
3 Blockade of PD-1 and PD-L2 reversed the reduced production of TNF-alpha and IFN-gamma induced by indomethacin in gammadelta T cells. Indomethacin programmed cell death 1 Mus musculus
4 In addition, long-term use of indomethacin activates TRIF/NF-kappaB and JAK/STAT3 pathways, and indomethacin promotes the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway respectively in gammadelta T cells. Indomethacin programmed cell death 1 Mus musculus
5 Given these findings, we drew a conclusion that long-term use of indomethacin leads to poor prognoses through promoting the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway to inhibit TNF-alpha and IFN-gamma in HCC. Indomethacin programmed cell death 1 Mus musculus