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Tumor cells have long been observed to share several biological characteristics with normal stem/progenitor cells; however, the oncogenic mechanisms underlying the lung stem/progenitor cell signaling remain elusive. Here, we report that  SOX2 , a self‐renewal factor in lung stem/progenitor cells, is highly expressed in a subclass of lung cancer cells, the proliferation, survival, and chemoresistance of which are dependent on SOX2 signaling. Overexpression of  SOX2  promotes oncogenic phenotypes in lung cancer cells; knockdown of  SOX2  attenuated cell proliferation. We observed that SOX2 increased the expression of epidermal growth factor receptor ( EGFR ), and EGFR activation further upregulated  SOX2  levels, forming a positive feedback loop. SOX2 expression promoted chemoresistance, and silencing of  SOX2  perturbed mitochondrial function, causing marked apoptosis and autophagy. SOX2 induced  BCL2L1 , the ectopic expression of which rescued the effects of  SOX2  silencing on apoptosis, autophagy, and mitochondrial function. SOX2 promoted tumor formation, along with increased cell proliferation in a xenograft mouse model. SOX2 expression is associated with poor prognosis in lung cancer patients; moreover,  SOX2 ,  EGFR , and  BCL2L1  expression levels were significantly correlated in lung tumors. Our findings support the emerging role of SOX2 in cell proliferation and survival by eliciting oncogenic EGFR and BCL2L1 signaling with potential applications as a prognosis marker and a therapeutic target in lung cancer. S tem  C ells   2013;31:2607–2619

The Emerging Role of SOX2 in Cell Proliferation and Survival and Its Crosstalk with Oncogenic Signaling in Lung Cancer