ArticlePloS one2013
Epithelial-mesenchymal transition (EMT) induced by TNF-α requires AKT/GSK-3β-mediated stabilization of snail in colorectal cancer.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.
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Who cites it
171 citing papers in PubMed.
- From Chronic Inflammation to Malignancy: Molecular Mechanisms and Therapeutic Insights in Oral Carcinogenesis.International journal of molecular sciences · 2026Review
- Association of Polymorphisms of Inflammatory-Relevant Genes with Cancer Risk.Current issues in molecular biology · 2026Article
- A Single-Cell Atlas of Uterine Carcinosarcoma from Diverse Ancestries.bioRxiv : the preprint server for biology · 2026Article
- High-Content SRS Imaging Unveils Altered Cholesterol Metabolism in Ovarian Cancers Under CAR-T Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microbial crosstalk along the oral-gut axis: organ-specific oncogenic adaptations of Porphyromonas gingivalis and Fusobacterium nucleatum.Neoplasia (New York, N.Y.) · 2026Review
- The Anti-EMMPRIN Monoclonal Antibody hMR18-mAb Induces Tumor Dormancy and Inhibits the EMT Process in Human Carcinoma Cell Lines Co-Cultured with Macrophages.Biomedicines · 2025Article
- TESMIN promotes lung adenocarcinoma proliferation, migration and invasion via PI3K/AKT/mTOR signaling.Scientific reports · 2025Article
- Targeting cytokine and chemokine signaling pathways for enhancing chemo-sensitivity in colorectal cancer.Cell communication and signaling : CCS · 2025Review
- Integrative single-cell transcriptomic analysis deciphers heterogeneous characteristics of gastrointestinal tract cancer.Clinical and translational medicine · 2025Article
- Mesenchymal stem cells-derived exosomes alleviate radiation induced pulmonary fibrosis by inhibiting the protein kinase B/nuclear factor kappa B pathway.World journal of stem cells · 2025Article
- Tumor Necrosis Factor-Alpha's Role in the Pathophysiology of Colon Cancer.Diseases (Basel, Switzerland) · 2025Review
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- Sequestration of ribosomal subunits as inactive 80S by targeting eIF6 limits mitotic exit and cancer progression.Nucleic acids research · 2025Article
- Mechanically induced development and maturation of 3DFrontiers in immunology · 2025Article
- Constructing a doxycycline-inducible system for an epithelial-to-mesenchymal transition model in MCF10A cells.Biology open · 2024Article
- Article
- Chaperone-mediated autophagy modulates Snail protein stability: implications for breast cancer metastasis.Molecular cancer · 2024Article
- IL-1β-activated PI3K/AKT and MEK/ERK pathways coordinately promote induction of partial epithelial-mesenchymal transition.Cell communication and signaling : CCS · 2024Article
- Ganglioside GD3 Regulates Inflammation and Epithelial-to-Mesenchymal Transition in Human Nasal Epithelial Cells.International journal of molecular sciences · 2024Article
111 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation-promoted metastasis has been considered as a major challenge in cancer therapy. Pro-inflammatory cytokine TNFα can induce cancer invasion and metastasis associated with epithelial-mesenchymal transition (EMT). However, the underlying mechanisms are not entirely clear. In this study, we showed that TNFα induces EMT in human HCT116 cells and thereby promotes colorectal cancer (CRC) invasion and metastasis. TNFα-induced EMT was characterized by acquiring mesenchymal spindle-like morphology and increasing the expression of N-cadherin and fibronectin with a concomitant decrease of E-cadherin and Zona occludin-1(ZO-1). TNFα treatment also increased the expression of transcription factor Snail, but not Slug, ZEB1 and Twist. Overexpression of Snail induced a switch from E-cadherin to N-cadherin expression in HCT116 cells, which is a characteristic of EMT. Conversely, knockdown of Snail significantly attenuated TNFα-induced EMT in HCT116 cells, suggesting that Snail plays a crucial role in TNFα-induced EMT. Interestingly, exposure to TNFα rapidly increased Snail protein expression and Snail nuclear localization but not mRNA level upregulation. Finally, we demonstrated that TNFα elevated Snail stability by activating AKT pathway and subsequently repressing GSK-3β activity and decreasing the association of Snail with GSK-3β. Knockdown of GSK-3β further verified our finding. Taken together, these results revealed that AKT/GSK-3β-mediated stabilization of Snail is required for TNFα-induced EMT in CRC cells. Our study provides a better understanding of inflammation-induced CRC metastasis.
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