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. Author manuscript; available in PMC: 2024 Mar 1.
Published in final edited form as: Mol Cancer Res. 2023 Sep 1;21(9):867–880. doi: 10.1158/1541-7786.MCR-22-1031

Figure 7. Model in which fibronectin contributes to a BRAF inhibitor-driven invasive phenotype through EGR1, which can be blocked by inhibition of ERK1/2.

Figure 7.

In response to BRAF inhibition, thyroid cancer cells resistant to BRAFi become more invasive. This invasive phenotype is accompanied by an increase in FN1 and a pro-invasive secretome. Inhibition of ERK1/2 prevents BRAFi-induced FN1 secretion and corresponding invasive phenotype and secretome. Combined BRAF and ERK1/2 inhibition results in decreased levels of EGR1, which is necessary for increased FN1 expression in response to BRAFi. FN1: fibronectin. BRAFi: dabrafenib. ERKi: SCH772984 or ulixertinib. Created with BioRender.com