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Chronic stress-induced cholesterol metabolism abnormalities promote ESCC tumorigenesis and predict neoadjuvant therapy response [RNA-Seq]

ABSTRACT: This project reported that chronic stress activates the GCR-HMGB2-LDLR axis via cortisol release, leading to abnormal cholesterol metabolism and ultimately promoting esophageal carcinogenesis. Chronic stress is associated with increased ESCC risk, and further exacerbates ESCC progression through HMGB2. Cortisol, by activating GCR, stimulates ESCC cell proliferation. Moreover, GCR activation enhances HMGB2 transcription, which in turn binds to SREBF1, thereby upregulating LDLR transcription and disrupting cholesterol metabolism. Clinical parameters in stressed ESCC patients underscore the relevance of stress management as a pivotal strategy for both the prevention and treatment of this malignancy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE286336 | GEO | 2025/01/14

REPOSITORIES: GEO

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Chronic stress-induced cholesterol metabolism abnormalities promote ESCC tumorigenesis and predict neoadjuvant therapy response

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