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

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

PROVIDER: PRJNA1208943 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31962739_1.fastq.gz	Fastqsanger.gz
	SRR31962739_2.fastq.gz	Fastqsanger.gz
	SRR31962740_1.fastq.gz	Fastqsanger.gz
	SRR31962740_2.fastq.gz	Fastqsanger.gz
	SRR31962741_1.fastq.gz	Fastqsanger.gz

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

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

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

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

Project description:Recent studies have demonstrated that chronic stress can enhance the development of multiple human diseases, including cancer. However, the role of chronic stress in esophageal carcinogenesis and its underlying molecular mechanisms remain unclear. This study uncovered that dysregulated cholesterol metabolism significantly promotes esophageal carcinogenesis under chronic stress conditions. Our findings indicate that the persistent elevation of glucocorticoids induced by chronic stress stimulates cho-lesterol uptake, contributing to esophageal carcinogenesis. The activated glucocor-ticoid receptor (GCR) enrichment at the promoter region of High Mobility Group Box Protein 2 (HMGB2) facilitates its transcription. As a transcription co-activator, HMGB2 enhances Sterol Regulatory Element-Binding Transcription Factor 1 (SREBF1) transcription and regulates cholesterol metabolism through LDL particle uptake into cells via Low-Density Lipoprotein Receptor (LDLR). These results em-phasize the significant impact of chronic stress on esophageal carcinogenesis and establish cholesterol metabolism disorder as a crucial link between chronic stress and the development of ESCC. The implications suggest that effectively managing chronic stress may serve as a viable strategy for preventing and treating ESCC.

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

Project description:chronic stress activates the GCR-HMGB2-LDLR axis via cortisol release, leading to abnormal cholesterol metabolism and ultimately promoting esophageal carcinogenesis

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