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In breast cancer, GPx2 is commonly overexpressed in the mammary carcinomas of mouse models of breast cancer induced by carcinogens, which is consistent with its up-regulation in human breast cancer [19]

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The mechanism of action involves binding to both GIP and GLP-1 receptors, which stimulates insulin secretion in a glucose-dependent manner, suppresses glucagon release, and promotes satiety

it invalidates the entire experiment