The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Tumor Immune Microenvironment during Epithelial–Mesenchymal Transition
Abstract
Epithelial–mesenchymal transition (EMT) has been shown to play a critical role in tumor development from initiation to metastasis. EMT could be regarded as a continuum, with intermediate hybrid epithelial and mesenchymal phenotypes having high plasticity. Classical EMT is characterized by the phenotype change of epithelial cells to cells with mesenchymal properties, but EMT is also associated with multiple other molecular processes, including tumor immune evasion. Some previous studies have shown that EMT is associated with the cell number of immunosuppressive cells, such as myeloid-derived suppressor cells, and the expression of immune checkpoints, such as programmed cell death-ligand 1, in several cancer types. At the molecular level, EMT transcriptional factors, including Snail, Zeb1, and Twist1, produce or attract immunosuppressive cells or promote the expression of immunosuppressive checkpoint molecules via chemokine production, leading to a tumor immunosuppressive microenvironment. In turn, immunosuppressive factors induce EMT in tumor cells. This feedback loop between EMT and immunosuppression promotes tumor progression. For therapy directly targeting EMT has been challenging, the elucidation of the interactive regulation of EMT and immunosuppression is desirable for developing new therapeutic approaches in cancer. The combination of immune checkpoint inhibitors and immunotherapy targeting immunosuppressive cells could be a promising therapy for EMT.
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Cites
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Chimeric Antigen Receptor T Cells for Sustained Remissions in Leukemia
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Cited by
Immunosuppressive cells in cancer: mechanisms and potential therapeutic targets
Tie, Y., Tang, F., Wei, Y.-Q., & Wei, X.-W. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01282-8 · Cited by 591
Allgayer, H., Mahapatra, S., Mishra, B., Swain, B., Saha, S., Khanra, S., Kumari, K., Panda, V. K., Malhotra, D., Patil, N. S., et al. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02338-2 · Cited by 127
Ramundo, V., Zanirato, G., & Aldieri, E. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222212216 · Cited by 46
Porter, R. L., Sun, S., Flores, M. N., Berzolla, E., You, E., Phillips, I. E., KC, N., Desai, N., Tai, E. C., Szabolcs, A., et al. (2022) · Journal of Clinical Investigation · doi:10.1172/jci155931 · Cited by 24
Fariha, F. T. J., Fuad, M., Saha, C. S., Hossen, S., & Hossain, M. J. (2025) · Scientific Reports · doi:10.1038/s41598-025-13315-6 · Cited by 1
Metadata
- Authors
- Taki, M., Abiko, K., Ukita, M., Murakami, R., Yamanoi, K., Yamaguchi, K., Hamanishi, J., Baba, T., Matsumura, N., & Mandai, M.
- Venue
- Clinical Cancer Research
- Published
- 2021-04-07
- Volume
- 27
- Issue
- 17
- Pages
- 4669-4679
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W3150492631
- Cited by
- 351
- References
- 23
- FWCI
- 18.92
- Type
- journal article
- Language
- en
- Open access
- closed
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