No abstract

No abstract

CAFs increases tumor growth while knockdown of CNTFR in lung tumor cells decreases overall growth. With the use of advanced protein engineering technology, we generated a high-affinity CNTFR decoy that inhibits CLCF1-CNTFR signaling and are currently testing this novel reagent to elucidate the mechanism by which CNTFR activation alters intercellular signaling to increase tumor cell growth. Through in vivo studies with cell lines and PDXs, we are also exploring the efficacy of this CNTFR decoy as a form of lung cancer therapy. Conclusion:In sum, these data indicate that CLCF1-CNTFR signaling is important for NSCLC tumor growth and is a viable therapeutic target.

No abstract