Psychological stress-driven modulation of YAP1 signaling: Mechanistic pathways linking stress biology to tumor progression

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Psychological distress is increasingly recognized as a biologically active contributor to cancer progression, and emerging evidence identifies yes-associated protein 1 (YAP1) as a central molecular node through which stress-related signaling influences tumor behavior. As a mechanosensitive transcriptional co-activator within the Hippo pathway, YAP1 integrates neuroendocrine, inflammatory, oxidative, and metabolic cues that become dysregulated under chronic stress, including cortisol elevation, sympathetic activation, pro-inflammatory cytokines, and reactive oxygen species. These stress-induced factors converge on Hippo-dependent and non-canonical regulators such as PI3K–AKT, Ras–MAPK, and integrin–FAK–RhoA, promoting YAP1 dephosphorylation, nuclear translocation, and oncogenic transcriptional activation. Enhanced YAP1 signaling drives proliferation, survival, metabolic rewiring, EMT, metastasis, immune evasion, and resistance to chemotherapy and immunotherapy, while also contributing to pain sensitization and inflammatory cascades. Together, these mechanisms suggest that YAP1 functions as a molecular bridge linking psychological stress with tumor progression, shaping both biological vulnerability and treatment responsiveness. Understanding how psychobiological stress modulates YAP1 opens opportunities for integrative strategies combining pharmacologic YAP1 targeting with psychological interventions that normalize cortisol rhythms, reduce inflammation, and restore autonomic balance, offering a novel framework for stress-responsive precision psycho-oncology.

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