
Melanoma is highly heterogeneous with diverse genomic alterations and partial therapeutic responses. The emergence of drug‐resistant tumor cell clones accompanied by a high AXL expression level is one of the major challenges for anti‐tumor clinical care. Recent studies have demonstrated that high AXL expression in melanoma cells mediated drug resistance, epithelial‐mesenchymal transition (EMT), and elevated survival of cancer stem cells (CSCs). Given that we have identified several non‐steroidal anti‐inflammatory drugs (NSAIDs) including aspirin potently induce the degradation of AXL, we questioned whether NSAIDs could counteract the AXL‐mediated neoplastic phenotypes...
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