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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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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

| PRJNA1208109 | ENA

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.

2025-01-13 | GSE286200 | GEO

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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MiRNA expression arrays from esophageal squamous cell carcinomas with different neoadjuvant chemoradiotherapy response

Project description:Preoperative chemoradiotherapy (CRT) followed by surgery has been proved to improve esophageal squamous cell carcinoma (ESCC) patients’ survival in comparison with surgery alone. However, the outcomes of CRT are heterogeneous, and no clinical or pathological method could predict CRT response. We aim to identify miRNA markers for ESCC CRT-response prediction through miRNA expression analyses. MiRNA expression analyses were performed on pretreatment cancer biopsies from 28 ESCCs who received neoadjuvant CRT and surgery using Agilent human miRNA microarrays based on miRBase (release 18.0) GeneChip®.

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Transcription profiling of human squamous cell carcinomas to predict response to neoadjuvant chemoradiotherapy in oesophageal cancer patients

Project description:To use gene expression profiles to predict response to neoadjuvant chemoradiotherapy in oesophageal cancer patients.

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Project description:Neoadjuvant therapy has been shown to improve survival for locally advanced esophageal squamous cell carcinoma (ESCC). However, some cases may acquire therapy resistance and the mechanism is still unclear. Here, we applied single-cell RNA sequencing on 7 ESCC patients with neoadjuvant therapy and 2 ESCC patients underwent general surgery alone to delineate the tumor heterogeneity, tumor microenvironment (TME) and potential hallmarks of therapy resistance. In total, 13 tumor cell lineages and its corresponding lineage-specific gene signatures, pathway activities, and transcription factors were identified, representing different mechanisms and hallmarks of neoadjuvant therapy resistance, such as oxidative stress response, hypoxia, DNA repair, ECM and EMT. Typically, tumor cell lineage Ep-C2 with signatures of oxidative stress response showed the strongest resistance to neoadjuvant therapy, particularly under chemoradiotherapy and immunotherapy combination. Excepting for the resistance mechanisms associated with tumor cell lineages, we also investigated three TME characteristics response to neoadjuvant therapy resistance, including the infiltration of cytotoxic-insufficient GZMK+ effector memory T cells, angiogenesis-promoting effect of myeloid lineages and the cell-cell communication of tumor-associated fibroblasts. These hallmarks of neoadjuvant therapy will help us to understand the therapy resistance in ESCC and provide important clues to identify potential targets to improve therapy sensitivity.

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