Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance
Epithelial to mesenchymal transition (EMT) contributes to tumor progression, cancer cell invasion, and therapy resistance. EMT is regulated by transcription factors such as the protein products of the SNAI gene family, which inhibits the expression of epithelial genes. Several signaling pathways, su...
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MDPI AG
2020-02-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/9/2/428 |
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| author | József Dudás Andrea Ladányi Julia Ingruber Teresa Bernadette Steinbichler Herbert Riechelmann |
| author_facet | József Dudás Andrea Ladányi Julia Ingruber Teresa Bernadette Steinbichler Herbert Riechelmann |
| author_sort | József Dudás |
| collection | DOAJ |
| description | Epithelial to mesenchymal transition (EMT) contributes to tumor progression, cancer cell invasion, and therapy resistance. EMT is regulated by transcription factors such as the protein products of the SNAI gene family, which inhibits the expression of epithelial genes. Several signaling pathways, such as TGF-beta1, IL-6, Akt, and Erk1/2, trigger EMT responses. Besides regulatory transcription factors, RNA molecules without protein translation, micro RNAs, and long non-coding RNAs also assist in the initialization of the EMT gene cluster. A challenging novel aspect of EMT research is the investigation of the interplay between tumor microenvironments and EMT. Several microenvironmental factors, including fibroblasts and myofibroblasts, as well as inflammatory, immune, and endothelial cells, induce EMT in tumor cells. EMT tumor cells change their adverse microenvironment into a tumor friendly neighborhood, loaded with stromal regulatory T cells, exhausted CD8<sup>+</sup> T cells, and M2 (protumor) macrophages. Several EMT inhibitory mechanisms are instrumental in reversing EMT or targeting EMT cells. Currently, these mechanisms are also significant for clinical use. |
| first_indexed | 2024-03-12T07:05:01Z |
| format | Article |
| id | doaj.art-3c00e876a30e4594b86e89b4ac69b1e8 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-12T07:05:01Z |
| publishDate | 2020-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-3c00e876a30e4594b86e89b4ac69b1e82023-09-02T23:28:14ZengMDPI AGCells2073-44092020-02-019242810.3390/cells9020428cells9020428Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/ChemoresistanceJózsef Dudás0Andrea Ladányi1Julia Ingruber2Teresa Bernadette Steinbichler3Herbert Riechelmann4Department of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, 6020 Innsbruck, AustriaDepartment of Surgical and Molecular Pathology, National Institute of Oncology, 1122 Budapest, HungaryDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, 6020 Innsbruck, AustriaDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, 6020 Innsbruck, AustriaDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, 6020 Innsbruck, AustriaEpithelial to mesenchymal transition (EMT) contributes to tumor progression, cancer cell invasion, and therapy resistance. EMT is regulated by transcription factors such as the protein products of the SNAI gene family, which inhibits the expression of epithelial genes. Several signaling pathways, such as TGF-beta1, IL-6, Akt, and Erk1/2, trigger EMT responses. Besides regulatory transcription factors, RNA molecules without protein translation, micro RNAs, and long non-coding RNAs also assist in the initialization of the EMT gene cluster. A challenging novel aspect of EMT research is the investigation of the interplay between tumor microenvironments and EMT. Several microenvironmental factors, including fibroblasts and myofibroblasts, as well as inflammatory, immune, and endothelial cells, induce EMT in tumor cells. EMT tumor cells change their adverse microenvironment into a tumor friendly neighborhood, loaded with stromal regulatory T cells, exhausted CD8<sup>+</sup> T cells, and M2 (protumor) macrophages. Several EMT inhibitory mechanisms are instrumental in reversing EMT or targeting EMT cells. Currently, these mechanisms are also significant for clinical use.https://www.mdpi.com/2073-4409/9/2/428silibininmrx34pd-l1nrf2krüppel-like factors (klfs)neurotrophin |
| spellingShingle | József Dudás Andrea Ladányi Julia Ingruber Teresa Bernadette Steinbichler Herbert Riechelmann Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance Cells silibinin mrx34 pd-l1 nrf2 krüppel-like factors (klfs) neurotrophin |
| title | Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance |
| title_full | Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance |
| title_fullStr | Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance |
| title_full_unstemmed | Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance |
| title_short | Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance |
| title_sort | epithelial to mesenchymal transition a mechanism that fuels cancer radio chemoresistance |
| topic | silibinin mrx34 pd-l1 nrf2 krüppel-like factors (klfs) neurotrophin |
| url | https://www.mdpi.com/2073-4409/9/2/428 |
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