Skip to main content
Fig. 4 | Cancer Cell International

Fig. 4

From: Epigenetic modification and BRAF gene mutation in thyroid carcinoma

Fig. 4

Different signaling pathways and BRAF inhibitors in thyroid cancer. BRAF and ERK1/2 inhibitors (SCH772984) reduce the activity of the MARK signaling pathway and inhibit ERK1/2 phosphorylation and activity, thereby inhibiting the growth of TC cells. BRAF inhibitor PLX4720 activates ULK1 by activating AMPK-ULK1 and inhibits autophagy, which promotes the death of TC cells. PLX4032 and vitamin C enhances the activity of PLX4032 in the body, thereby reducing the abnormal activation of MAPK/ERK and PI3K/AKT pathways, blocking the G2/M phase of TC cells, and inducing BRAFV600E mutant TC cell apoptosis. NSAIDs can reverse the activity of this protein and inhibit the expression of cyclin D1, matrix metalloproteinases, c-myc, and other oncogenic factors, thereby reducing the invasion ability of BRAFV600E mutant tumors. SPYR1 activates the MAPK/PI3K/AKT pathway to promote tumour cell growth. The hypermethylation of the PTEN and DAPK inactivating the P13K/Akt and MAPK signaling pathway promoted TC cell growth

Back to article page