fig1

Stress and drug resistance in cancer

Figure 1. Stress hormone mechanism of action. The HPA signals the release of glucocorticoids. Activation of the GR mediates transactivation and transrepression of genes through binding to the GRE, which controls the expression of genes involved in inflammation, survival and apoptosis. Stimulation of the SNS promotes the release of catecholamines. Activation of the BADR by adrenaline/noradrenaline stimulates synthesis of cAMP which in turn activates PKA. Phosphorylation of a number of PKA-receptive proteins involved in cell survival, proliferation and gene transcription can then occur. HPA: hypothalamic-pituitary-axis; GR: glucocorticoid receptor; GRE: glucocorticoid response element; SNS: sympathetic nervous system; BADR: beta-adrenergic receptor; cAMP: cyclic adenosine monophosphate; PKA: protein kinase A

Cancer Drug Resistance
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