The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Epithelial–Mesenchymal Transition (EMT) Induced by TNF-α Requires AKT/GSK-3β-Mediated Stabilization of Snail in Colorectal Cancer
Open accessAbstract
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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Cites
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“Snail is Crucial for TNFa-mediated EMT Since transcription factors Snail, ZEB1, Twist and Slug play essential roles in regulating EMT [14], we then investigated whether their expressions were up-regulated in HCT116 cells after treated with TNFa.”
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Cited by
Zhang, F., Wang, H., Wang, X., Jiang, G., Liu, H., Zhang, G., Wang, H., Fang, R., Bu, X., Cai, S., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.10561 · Cited by 580
Self-citationEpithelial–mesenchymal transition in colorectal cancer metastasis: A system review
Cao, H., Xu, E., Liu, H., Wan, L., & Lai, M. (2015) · Pathology - Research and Practice · doi:10.1016/j.prp.2015.05.010 · Cited by 356
Immunity, Hypoxia, and Metabolism–the Ménage à Trois of Cancer: Implications for Immunotherapy
Riera-Domingo, C., Audigé, A., Granja, S., Cheng, W.-C., Ho, P.-C., Baltazar, F., Stockmann, C., & Mazzone, M. (2020) · Physiological Reviews · doi:10.1152/physrev.00018.2019 · Cited by 310
Pretzsch, E., Bösch, F., Neumann, J., Ganschow, P., Bazhin, A., Guba, M., Werner, J., & Angele, M. (2019) · Journal of Oncology · doi:10.1155/2019/7407190 · Cited by 298
Environmental immune disruptors, inflammation and cancer risk
Thompson, P. A., Khatami, M., Baglole, C. J., Sun, J., Harris, S. A., Moon, E.-Y., Al-Mulla, F., Al-Temaimi, R., Brown, D. G., Colacci, A. M., et al. (2015) · Carcinogenesis · doi:10.1093/carcin/bgv038 · Cited by 227
Metadata
- Authors
- Wang, H., Wang, H.-S., Zhou, B.-H., Li, C.-L., Zhang, F., Wang, X.-F., Zhang, G., Bu, X.-Z., Cai, S.-H., & Du, J.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-02-19
- Volume
- 8
- Issue
- 2
- Pages
- e56664
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1987380441
- Cited by
- 273
- References
- 50
- FWCI
- 13.75
- Type
- journal article
- Language
- en
- Open access
- gold
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- The paper
- Wang, H., Wang, H.-S., Zhou, B.-H., Li, C.-L., Zhang, F., Wang, X.-F., Zhang, G., Bu, X.-Z., Cai, S.-H., & Du, J. (2013). Epithelial–Mesenchymal Transition (EMT) Induced by TNF-α Requires AKT/GSK-3β-Mediated Stabilization of Snail in Colorectal Cancer. PLoS ONE. https://doi.org/10.1371/journal.pone.0056664
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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