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Fig. 7 | Breast Cancer Research

Fig. 7

From: Foxf2 plays a dual role during transforming growth factor beta-induced epithelial to mesenchymal transition by promoting apoptosis yet enabling cell junction dissolution and migration

Fig. 7

Schematic model of the dual role of Foxf2 during TGFβ-induced EMT. Receptor activation by transforming growth factor (TGF)β leads to phosphorylation of receptor-bound Smads with subsequent Smad complex formation. The trimeric complex enters the nucleus to activate the expression of TGFβ target genes, such as the forkhead transcription factor Foxf2. Subsequently, Foxf2 directly represses the transcription of the epidermal growth factor (EGFR) ligands betacellulin (Btc) and amphiregulin (Areg), which leads to reduced EGFR-mediated survival signaling. Furthermore, Foxf2 transcriptionally activates the proapoptotic gene Noxa, resulting in the induction of caspase-dependent apoptosis. On the other hand, downregulation of E-cadherin (Ecad) is modulated by Foxf2-dependent upregulation of Zeb1/Zeb2, downregulation of Id2, and a double-negative feedback loop between Foxf2 and the miR-200 family, leading to the disruption of adherens junctions and the subsequent increase in cell migration

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Breast Cancer Research

ISSN: 1465-542X

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