Targeting LINC01711 in FAP+ cancer-associated fibroblasts overcomes lactate-mediated immunosuppression and enhances anti-PD-1 efficacy in lung adenocarcinoma



Summary

Targeting LINC01711 in cancer-associated fibroblasts (CAFs) expressing fibroblast activation protein (FAP) shows promise in overcoming immunosuppression in lung adenocarcinoma. Researchers discovered that LINC01711 promotes lactate production by FAP+ CAFs, fueling tumor cells and suppressing immune cell activity. Blocking LINC01711 reduces lactate secretion, restoring immune cell function and increasing tumor sensitivity to anti-PD-1 therapy. This suggests that inhibiting LINC01711 could enhance the effectiveness of immunotherapy by disrupting the lactate-mediated immunosuppressive environment created by FAP+ CAFs in lung adenocarcinoma.

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