Transcription factor glioma-associated oncogene homolog 1 is required for transforming growth factor-ß1-induced epithelial-mesenchymal transition of non-small cell lung cancer cells.

Epithelial­mesenchymal transition (EMT) is the process by which epithelial cells depolarize and acquire a mesenchymal phenotype, and is a common early step in the process of metastasis. Patients with lung cancer frequently already have distant metastases when they are diagnosed, highlighting the requirement for early and effective interventions to control metastatic disease. Transforming growth factor­ß1 (TGF­ß1) is able to induce EMT, however the molecular mechanism of this remains unclear. In the current study, TGF­ß1 was reported to induce EMT and promote the migration of non­small cell lung cancer (NSCLC) cells. A notable observation was that EMT induction was accompanied by the upregulation of human glioma­associated oncogene homolog 1 (Gli1) mRNA and protein levels. Furthermore, Gli1 levels were depleted by small interfering RNA, and the Gli1 inhibitor GANT 61 attenuated the TGF­ß1­mediated induction of EMT and cell migration. The results of the current study suggest that Gli1 regulates TGF­ß1­induced EMT, which may provide a novel therapeutic target to inhibit metastasis in patients with NSCLC.