Transcriptional activation of NANOG by YBX1 promotes lung cancer stem-like properties and metastasis

population. Conversely, reduced YBX1 impaired CSC properties of NSCLC cells in vitro and tumor-initiating frequencies, as well as metastasis in vivo. Importantly, we described a mechanism whereby YBX1 directly promoted NANOG, a transcription factor, transcriptional activation. Depletion of NANOG abolished the enhanced ability of invasion and sphere formation in YBX1 elevated-A549 cells. Collectively, these findings demonstrate a novel role of YBX1 in maintaining the stemness of CSCs and metastasis, unveiling YBX1 as promising therapeutic target for NSCLC treatments.