ArticleMedical oncology (Northwood, London, England)2012
Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma.
Article in Medical oncology (Northwood, London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- How to efficiently establish animal models of cholangiocarcinoma: challenges and inspiration.Medical review (2021) · 2026Review
- Initial drainage-related prognostic factors for perihilar cholangiocarcinoma: A single-center retrospective study.DEN open · 2023Article
- IFIT2 Depletion Promotes Cancer Stem Cell-like Phenotypes in Oral Cancer.Biomedicines · 2023Article
- The contradictory roles of macrophages in non-alcoholic fatty liver disease and primary liver cancer-Challenges and opportunities.Frontiers in molecular biosciences · 2023Review
- Tumor microenvironment enriches the stemness features: the architectural event of therapy resistance and metastasis.Molecular cancer · 2022Review
- Similarities and differences among the Opisthorchiidae liver flukes: insights fromParasitology · 2022Review
- A comparative study on the model of PMEnvironmental science and pollution research international · 2022Article
- The mechanism of lncRNAs in the crosstalk between epithelial-mesenchymal transition and tumor microenvironment for early colon adenocarcinoma based on molecular subtyping.Frontiers in genetics · 2022Article
- Berberine as a potential agent for breast cancer therapy.Frontiers in oncology · 2022Review
- LIN28B Enhanced STAT3 Signaling Regulates Inflammatory Response and Chemotherapeutic Resistance in Cholangiocytes.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Metformin suppressed tumor necrosis factor-α-induced epithelial-mesenchymal transition in prostate cancer by inactivating the NF-κB signaling pathway.Translational cancer research · 2020Article
- Periostin induces epithelial‑to‑mesenchymal transition via the integrin α5β1/TWIST‑2 axis in cholangiocarcinoma.Oncology reports · 2020Article
- Role of Cancer Stem Cells in Cholangiocarcinoma and Therapeutic Implications.International journal of molecular sciences · 2019Review
- Ponicidin inhibits pro-inflammatory cytokine TNF-α-induced epithelial-mesenchymal transition and metastasis of colorectal cancer cells via suppressing the AKT/GSK-3β/Snail pathway.Inflammopharmacology · 2019Article
- Melatonin preconditioning of bone marrow-derived mesenchymal stem cells promotes their engraftment and improves renal regeneration in a rat model of chronic kidney disease.Journal of molecular histology · 2019Article
- PMFrontiers in physiology · 2019Review
- The role of tumour microenvironment: a new vision for cholangiocarcinoma.Journal of cellular and molecular medicine · 2019Review
- Relationship between epithelial-to-mesenchymal transition and the inflammatory microenvironment of hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2018Review
- Article
- Cancer; an induced disease of twentieth century! Induction of tolerance, increased entropy and 'Dark Energy': loss of biorhythms (Anabolism v. Catabolism).Clinical and translational medicine · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a series of events during which epithelial cells lose many of their epithelial characteristics and take on properties that are typical of mesenchymal cells that lack cell-cell adhesion properties. EMT may be activated by various types of growth factors or inflammatory cytokines. In many types of epithelial cancers, the EMT-derived tumor cells are susceptible to metastasis. During tumor progression, epithelial cells acquire a gene expression pattern closely resembling that of mesenchymal cells. This study aimed to investigate the expression of the EMT-associated transcription factor Snail and an adhesion molecule E-cadherin in cholangiocarcinoma (CCA) tissues. The effect of TNF-α on EMT activation in CCA cells was also demonstrated. The qRT-PCR analysis revealed that Snail expression significantly increased in CCA (P = 0.01) and was correlated with tumor metastasis (P = 0.02). The expression of Snail was inversely associated with E-cadherin (P = 0.004). The stimulation of TNF-α enhances migration behavior and showed significantly induced expression of Snail in CCA cell lines, whereas expression of E-cadherin and CK-19 (the epithelial marker) was reduced. Immunofluorescence analysis revealed that TNF-α-treated CCA cell lines increased nuclear translocation of Snail, whereas E-cadherin was dramatically decreased. Our findings suggest that the changes in the expression of Snail or E-cadherin might regulate EMT development in CCA resulting in promoting tumor progression. Overexpression of Snail could be used as a prognostic marker for monitoring the treatment efficiency of CCA patients.
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