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. 2009 Sep 1;119(10):3127–3137. doi: 10.1172/JCI38543

Figure 6. Increased FOXN1 expression in SCC cells induces FGFR3 expression and promotes differentiation.

Figure 6

(A) The keratinocyte-derived SCC cell lines SCC13 and SCCO28 were infected with a retrovirus expressing FOXN1-ER fusion protein (34) or empty vector control. Cells with or without 200 nM 4-OHT treatment for 24 hours were analyzed, in parallel with control human keratinocytes, for levels of FOXN1 expression by immunoblotting, with γ-tubulin for equal loading control. Endogenous FOXN1 was detected at 69 kDa, and the higher–molecular weight band in the SCC cells corresponds to expression of the FOXN1-ER fusion protein. Lanes were run on the same gel but were noncontiguous (white line). (B–D) SCC13 and SCCO28 cells infected with the FOXN1-ER retrovirus or empty vector control were treated with 200 nM 4-OHT for 24 hours to induce activation of FOXN1-ER. Expression of involucrin (B), keratin1 (C), and FGFR3 (D) was analyzed by real-time RT-PCR using 36B4 for normalization. Error bars denote SEM. (E) SCCO28 cells were transduced with a FOXN1-expressing adenovirus (41) or GFP control and analyzed for expression of FGFR3 and keratin1 by immunoblotting, with γ-tubulin for equal loading control. Results were quantified by densitometric scanning of the immunoblots and normalization for γ-tubulin.