Given that we have previously demonstrated that SP1 mediates upregulation of the potential stem cell marker, ABCG2 in lung tumor cells following CSC exposure [41], we questioned if SP1 also contributes to CSC-mediated activation of ZFAS1. qRT-PCR assays demonstrated that endogenous levels of SP1 mRNA were higher in lung cancer cells compared with NREC; consistent with our previous observations in esophageal cancer [42], cigarette smoke did not increase SP1 expression in lung cancer cells (Fig. 10A). This evidence concerns the gene SP1 and lung carcinoma.