ArticleCurrent medicinal chemistry2013
Indometacin ameliorates high glucose-induced proliferation and invasion via modulation of e-cadherin in pancreatic cancer cells.
Article in Current medicinal chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Metabolic changes in neuroendocrine neoplasms.Cellular and molecular life sciences : CMLS · 2025Review
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- Chemotherapy and Physical Therapeutics Modulate Antigens on Cancer Cells.Frontiers in immunology · 2022Review
- Review
- Article
- Metalloporphyrin-indomethacin conjugates as new photosensitizers for photodynamic therapy.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2019Article
- Novel agents for pancreatic ductal adenocarcinoma: emerging therapeutics and future directions.Journal of hematology & oncology · 2018Review
- Glucose insult elicits hyperactivation of cancer stem cells through miR-424-cdc42-prdm14 signalling axis.British journal of cancer · 2017Article
- Article
- Glucose promotes cell proliferation, glucose uptake and invasion in endometrial cancer cells via AMPK/mTOR/S6 and MAPK signaling.Gynecologic oncology · 2015Article
- Tumour-suppressive function of SIRT4 in human colorectal cancer.British journal of cancer · 2015Article
- Downregulation of FAP suppresses cell proliferation and metastasis through PTEN/PI3K/AKT and Ras-ERK signaling in oral squamous cell carcinoma.Cell death & disease · 2014Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Indometacin, an inhibitor of cyclooxygenase-2 (COX-2), has been shown to exert anticancer effects in a variety of cancers. However, the effect and mechanism of indometacin on high glucose (HG)-induced proliferation and invasion of pancreatic cancer (PC) cells remain unclear. Multiple lines of evidence suggest that a large portion of pancreatic cancer (PC) patients suffer from either diabetes or HG which contributing PC progression. In this study, we report that indometacin down-regulated HG-induced proliferation and invasion via up-regulating E-cadherin but not COX-2 in PC cells. Additionally, the E-cadherin transcriptional repressors, Snail and Slug, were also involved in the process. Furthermore, the proliferation and invasion of PC cells, incubated in HG medium and treated with indometacin were significantly increased when E-cadherin was knocked down (Si-E-cad). Moreover, the protein levels of MMP-2, MMP-9, and VEGF were increased in PC cells transfected with Si-E-cad. Finally, the activation of the PI3K/AKT/GSK-3β signaling pathway was demonstrated to be involved in indometacin reversing HG-induced cell proliferation and invasion in PC cells. In conclusion, these results suggest that indometacin plays a key role in down-regulating HG-induced proliferation and invasion in PC cells. Our findings indicate that indometacin could be used as a novel therapeutic strategy to treat PC patients who simultaneously suffer from diabetes or HG.
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