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

GSE286336 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/01/14 Platform GPL34284
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE286336_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1208943 and SRA study SRP556601. Searching any of these in the dataset finder brings you back here.

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