ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Cancer-related inflammation and Barrett's carcinogenesis: interleukin-6 and STAT3 mediate apoptotic resistance in transformed Barrett's cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 70 citations in OpenAlex.
- Treatment of non-erosive reflux disease and dynamics of the esophageal microbiome: a prospective multicenter study.Scientific reports · 2020Trial
- Circulating Inflammation Biomarkers and the Risk of Esophageal Adenocarcinoma: A Nested Case-Control Study in the Department of Defense Serum Repository.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
- Attenuation of esophageal anastomotic stricture through remote ischemic conditioning in a rat model.Scientific reports · 2024Article
- Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett's Esophagus.Cancers · 2023Article
- Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma.International journal of molecular sciences · 2023Review
- Pan-cancer analysis andFrontiers in oncology · 2023Article
- Augmented CPT1A Expression Is Associated with Proliferation and Colony Formation during Barrett's Tumorigenesis.International journal of molecular sciences · 2022Article
- The antioxidant response in Barrett's tumorigenesis: A double-edged sword.Redox biology · 2021Review
- Article
- Chemoprevention of esophageal adenocarcinoma.Gastroenterology report · 2020Review
- Research progress of cancer stem cells and IL-6/STAT3 signaling pathway in esophageal adenocarcinoma.Translational cancer research · 2020Review
- Article
- Esophageal Microenvironment: From Precursor Microenvironment to Premetastatic Niche.Cancer management and research · 2020Review
- Cystatin F involvement in adenosine AScientific reports · 2018Article
- siRNA Library Screening Identifies a Druggable Immune-Signature Driving Esophageal Adenocarcinoma Cell Growth.Cellular and molecular gastroenterology and hepatology · 2018Article
- MicroRNA profile in neosquamous esophageal mucosa following ablation of Barrett's esophagus.World journal of gastroenterology · 2017Article
- Recent Advances in Aptamers Targeting Immune System.Inflammation · 2017Review
- STAT3 signaling drives EZH2 transcriptional activation and mediates poor prognosis in gastric cancer.Molecular cancer · 2016Article
- The tumor microenvironment in esophageal cancer.Oncogene · 2016Review
- Broad targeting of resistance to apoptosis in cancer.Seminars in cancer biology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer-related inflammation recently has been proposed as a major physiological hallmark of malignancy. Some genetic alterations known to promote cellular proliferation and induce malignant transformation also may participate in an intrinsic inflammatory pathway that produces a cancer-promoting inflammatory microenvironment. Little is known about this intrinsic inflammatory pathway in Barrett's esophagus. We have used a series of nontransformed and transformed human Barrett's epithelial cell lines developed in our laboratory to explore the potential contribution of interleukin (IL)-6 and signal transducer and activator of transcription (STAT3) (key molecules in the intrinsic inflammatory pathway) to Barrett's carcinogenesis. We determined IL-6 mRNA expression and protein secretion and protein expression of activated phospho-STAT3 and its downstream target myeloid cell leukemia (mcl)-1 (Mcl-1). We used an IL-6 blocking antibody and two JAK kinase inhibitors (AG490 and JAK inhibitor I) to assess whether STAT3 activation is IL-6 dependent. We also used small interfering RNAs (siRNAs) to STAT3 and Mcl-1 to assess effects of STAT3 pathway inhibition on apoptosis. Phospho-STAT3 was expressed only by transformed Barrett's cells, which also exhibited higher levels of IL-6 mRNA and of IL-6 and Mcl-1 proteins than nontransformed Barrett's cells. STAT3 phosphorylation could be blocked by IL-6 blocking antibody and by AG490 and JAK inhibitor I. In transformed Barrett's cells, rates of apoptosis following exposure to deoxycholic acid were significantly increased by transfection with siRNAs for STAT3 and Mcl-1. We conclude that activation of the IL-6/STAT3 pathway in transformed Barrett's epithelial cells enables them to resist apoptosis. These findings demonstrate a possible contribution of the intrinsic inflammatory pathway to carcinogenesis in Barrett's esophagus.
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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.