ArticleOncogene2012
Dietary zinc deficiency fuels esophageal cancer development by inducing a distinct inflammatory signature.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- A comprehensive analysis of mRNA expression profiles of Esophageal Squamous Cell Carcinoma reveals downregulation of Desmoglein 1 and crucial genomic targets.Cancer biomarkers : section A of Disease markers · 2023Pooled it
- TLR4 promotes ESCC progression by driving inflammation and metabolic reprogramming through SLC39A10-mediated zinc homeostasis.Journal of translational medicine · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Review
- Association between preoperative serum zinc level and prognosis in patients with advanced esophageal cancer in the neoadjuvant treatment era.Annals of gastroenterological surgery · 2024Article
- Zinc Deficiency as a General Feature of Cancer: a Review of the Literature.Biological trace element research · 2024Review
- Co-exposure to iron, copper, zinc, selenium and titanium is associated with the prevention of gastric precancerous lesions.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Global comparative transcriptomes uncover novel and population-specific gene expression in esophageal squamous cell carcinoma.Infectious agents and cancer · 2023Article
- Zinc treatment reverses and anti-Zn-regulated miRs suppress esophageal carcinomas in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Construction of a prognostic model for colorectal adenocarcinoma based on Zn transport-related genes identified by single-cell sequencing and weighted co-expression network analysis.Frontiers in oncology · 2023Article
- Zinc's Association with the CmPn/CmP Signaling Network in Breast Cancer Tumorigenesis.Biomolecules · 2022Review
- Article
- Esophagus cancer and essential trace elements.Frontiers in public health · 2022Review
- Aberrance of Zinc Metalloenzymes-Induced Human Diseases and Its Potential Mechanisms.Nutrients · 2021Review
- Microarray Analysis of the Chemoprophylaxis Effect of Zinc Gluconate: Inspiring but Caution Required.Digestive diseases and sciences · 2021Article
- Effects of dietary zinc deficiency on esophageal squamous cell proliferation and the mechanisms involved.World journal of gastrointestinal oncology · 2021Article
- Review
- Celecoxib alleviates zinc deficiency-promoted colon tumorigenesis through suppressing inflammation.Aging · 2021Article
- Natural Agents Targeting Mitochondria in Cancer.International journal of molecular sciences · 2020Review
- Zinc dysregulation in cancers and its potential as a therapeutic target.Cancer biology & medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic inflammation is implicated in the pathogenesis of esophageal squamous cell carcinoma (ESCC). The causes of inflammation in ESCC, however, are undefined. Dietary zinc (Zn)-deficiency (ZD) increases the risk of ESCC. We have previously shown that short-term ZD (6 weeks) in rats induces overexpression of the proinflammatory mediators S100a8 and S100a9 in the esophageal mucosa with accompanying esophageal epithelial hyperplasia. Here we report that prolonged ZD (21 weeks) in rats amplified this inflammation that when combined with non-carcinogenic low doses of the environmental carcinogen, N-nitrosomethylbenzylamine (NMBA) elicited a 66.7% (16/24) incidence of ESCC. With Zn-sufficiency, NMBA produced no cancers (0/21) (P<0.001). At tumor endpoint, the neoplastic ZD esophagus, as compared with Zn-sufficient esophagus, had an inflammatory gene signature with upregulation of numerous cancer-related inflammation genes (CXC and CC chemokines, chemokine receptors, cytokines and Cox-2) in addition to S100a8 and S100a9. This signature was already activated in the earlier dysplastic stage. Additionally, time-course bioinformatics analysis of expression profiles at tumor endpoint and before NMBA exposure revealed that this sustained inflammation was due to ZD rather than carcinogen exposure. Importantly, Zn replenishment reversed this inflammatory signature at both the dysplastic and neoplastic stages of ESCC development, and prevented cancer formation. Thus, the molecular definition of ZD-induced inflammation as a critical factor in ESCC development has important clinical implications with regard to development and prevention of this deadly disease.
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Registered trials
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.