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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: Role of thyroid hormone-integrin αvβ3-signal and therapeutic strategies in colorectal cancers

Fig. 2

Targeting Therapies of CRC is compensated by NDAT in K-Ras Mutant Colorectal Cancers. Thyroid hormone stimulates signal pathway of integrin αvβ3-FAK axis and proliferation. EGF via EGFR-Ras pathway promotes proliferation. It also cross-talks with integrin αvβ3 signal via FAK activation. These signals can induce activation of PI3K- and ERK1/2-dependent pathways. In addition, signals via growth factor receptors are also able to induce β-catenin-dependent cell proliferation. NDAT inhibits signal pathway of integrin αvβ3-FAK axis and proliferation. EGFR-dependent signal pathways via Ras-PI3K/ERK1/2 crosstalk with FAK. These signals can be intercepted by blocking activation of FAK, PI3K and ERK1/2. Crosstalk between growth factor receptors and FAK can be blocked by NDAT treatment

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