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SOX2 is a transcription factor essential for early mammalian development and for the maintenance of stem cells. Recently, SOX2 was identified as a lineage specific oncogene, recurrently amplified and activated in lung and esophageal squamous cell carcinoma (SCC). In this study, we have developed a zinc finger-based artificial transcription factor (ATF) to selectively suppress SOX2 expression in cancer cells and termed the system ATF/ SOX2 . We engineered the ATF using six zinc finger arrays designed to target a 19 bp site in the SOX2 distal promoter and a KOX transcriptional repressor domain. A recombinant adenoviral vector Ad-ATF/ SOX2 that expresses ATF/ SOX2 suppressed SOX2 at the mRNA and protein levels in lung and esophageal SCC cells expressing SOX2. In these kinds of cells, Ad-ATF/ SOX2 decreased cell proliferation and colony formation more effectively than the recombinant adenoviral vector Ad-sh SOX2 , which expresses SOX2 short hairpin RNA (sh SOX2 ). Ad-ATF/ SOX2 induced the cell cycle inhibitor CDKN1A more strongly than Ad-sh SOX2 . Importantly, the ATF did not suppress the cell viability of normal human cells. Moreover, Ad-ATF/ SOX2 effectively inhibited tumor growth in a lung SCC xenograft mouse model. These results indicate that ATF/ SOX2 would lead to the development of an effective molecular-targeted therapy for lung and esophageal SCC.

Targeted silencing of SOX2 by an artificial transcription factor showed antitumor effect in lung and esophageal squamous cell carcinoma