Figure 5.

The MAPK/ERK signaling pathway and its role in cancer development. The pathway governs cell proliferation, survival, and metastasis through interactions among key proteins and enzymes like SRC, KRAS, BRAF, MEK1/2, and ERK1/2. Increased activation (green) and expression (yellow) of pathway components often lead to uncontrolled cell growth and cancer progression. Mutations, such as KRAS mutations in colorectal cancer and BRAF^V600E mutations in melanoma and colorectal cancer, hyperactivate the pathway, promoting tumorigenesis and metastasis. Loss of the tumor suppressor gene PTEN (red) activates the PI3K/AKT pathway, contributing to cancer progression by enhancing cell proliferation and survival. DUSP4, a negative regulator of ERK1/2, may experience copy number loss, diminishing its ability to control pathway activity. The intricate nature of the MAPK/ERK pathway and its crosstalk with other signaling pathways highlight the importance of targeted therapies to disrupt these interactions and effectively combat cancer.