Abstract
Lung adenocarcinoma (ADC) to squamous cell carcinoma (SCC) transdifferentiation (AST) has been consistently observed in the clinic and associates with drug resistance in molecular targeted therapy. Our previous studies have demonstrated that LKB1 deficiency is an important trigger for AST process in the KrasG12D/Lkb1L/L (KL) genetically engineered mouse model (GEMM). However, there remains largely unknown about other factors than LKB1 in contributing to AST. Using the KrasG12D/Trp53L/L (KP) mouse model known to produce lung ADC only, we find that long-term treatments with the inhibitors of lysyl oxidase (LOX) sufficiently deplete collagen deposition and drive the AST process.
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