Final answer:
A mutated RAS protein that loses GTPase activity leads to unregulated phosphorylation cascades, causing uncontrolled cell proliferation and potentially cancer. These mutations can cause continuous activation of signaling pathways, leading to tumor growth and metastasis.
Step-by-step explanation:
When the RAS protein is mutated, leading to a loss in GTPase activity, it becomes unable to hydrolyze GTP into GDP. Normally, the RAS protein activates RAF, which then phosphorylates MEK, leading to the phosphorylation of ERK. The activated ERK enters the nucleus and triggers a response that can lead to cell proliferation and differentiation. However, when RAS mutations interfere with GTP hydrolysis, ERK gets continuously activated, leading to an unregulated phosphorylation cascade. This results in the activation of transcription factors that cause uncontrolled cell proliferation, a hallmark of cancer, because the cell's normal growth-regulating signals are overridden.
Cancer biologists have found that approximately 30% of all cancers may result from mutated RAS genes. These mutations can therefore lead to tumor growth and metastasis, the spread of cancer cells to new locations in the body. Understanding the role of RAS and its mutations is critical for developing treatments targeting these aberrant signaling pathways.