Evidence map›Paper›PMID 39869796›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

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

Ting Wang, Xiangyu Wang, Keke Wang, Mengyuan Yu, Ruihua Bai, Yiru Zhang, Zihan Zhang, Feifei Liu, Rui Wang, Xiaodan Shi and 6 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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  8. Review
  9. Chronic stress-induced cholesterol metabolism abnormalities promote ESCC tumorigenesis and predict neoadjuvant therapy response.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Ting Wang *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0009-0003-3537-7676
Xiangyu Wang *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0009-0001-3859-433X
Keke WangChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan 450000, China.ORCID 0000-0001-9256-2999
Mengyuan YuDepartment of Pathology, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan 450000, China.ORCID 0009-0002-8426-3643
Ruihua BaiDepartment of Pathology, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan 450000, China.ORCID 0009-0002-6951-5582
Yiru ZhangDepartment of Pathology, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan 450000, China.ORCID 0009-0008-3769-4284
Zihan ZhangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0009-0006-1301-151X
Feifei LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0002-2825-733X
Rui WangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0009-0005-5790-8268
Xiaodan ShiChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan 450000, China.ORCID 0000-0002-8427-2120
Ludan JiaDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0009-0003-6187-0085
Kangdong LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0002-4425-5625
Xiang LiDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.
Guoguo JinChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan 450000, China.
Simin ZhaoChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan 450000, China.ORCID 0000-0002-1880-9612
Zigang DongDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0002-4174-4028

Funding

Key projects jointly built by Henan Province and the Ministry of Finance No. SBGJ202102068 No. SBGJ202102071 No. 242102311187 No. 242300420096MOST | NSFC | National Natural Science Foundation of China No. 82073075 No.81872335MOST | NSFC | National Natural Science Foundation of China No. 82203290
6 · The paper itself

Abstract

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 cholesterol uptake, contributing to esophageal carcinogenesis. The activated glucocorticoid receptor (GCR) enrichment at the promoter region of High Mobility Group Box 2 (HMGB2) facilitates its transcription. As a transcription coactivator, 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 emphasize 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.

Indexed as

CarcinogenesisCholesterolEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaStress, PhysiologicalAnimalsCell Line, TumorGene Expression Regulation, NeoplasticGlucocorticoidsHumansMaleMiceNeoadjuvant TherapyReceptors, GlucocorticoidReceptors, LDLCholesterolGlucocorticoidsReceptors, GlucocorticoidReceptors, LDLchronic stresscortisolESCCHMGB2LDLR

Identifiers

PMID39869796
PMCPMC11804521

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.