Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy
Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor,...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Open Exploration Publishing Inc.
2023-08-01
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| Series: | Exploration of Immunology |
| Subjects: | |
| Online Access: | https://www.explorationpub.com/Journals/ei/Article/1003108 |
| _version_ | 1797691849614295040 |
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| author | Sourio Chakraborty Sumon Mukherjee Udit Basak Subhadip Pati Apratim Dutta Saikat Dutta Subhanki Dhar Tania Sarkar Aharna Guin Gaurisankar Sa Tanya Das |
| author_facet | Sourio Chakraborty Sumon Mukherjee Udit Basak Subhadip Pati Apratim Dutta Saikat Dutta Subhanki Dhar Tania Sarkar Aharna Guin Gaurisankar Sa Tanya Das |
| author_sort | Sourio Chakraborty |
| collection | DOAJ |
| description | Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs. |
| first_indexed | 2024-03-12T02:19:18Z |
| format | Article |
| id | doaj.art-777ed888517245ccac0079cece460259 |
| institution | Directory Open Access Journal |
| issn | 2768-6655 |
| language | English |
| last_indexed | 2024-03-12T02:19:18Z |
| publishDate | 2023-08-01 |
| publisher | Open Exploration Publishing Inc. |
| record_format | Article |
| series | Exploration of Immunology |
| spelling | doaj.art-777ed888517245ccac0079cece4602592023-09-06T06:32:55ZengOpen Exploration Publishing Inc.Exploration of Immunology2768-66552023-08-013438440510.37349/ei.2023.00108Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapySourio Chakraborty0https://orcid.org/0000-0003-4925-2754Sumon Mukherjee1https://orcid.org/0000-0003-2175-0348Udit Basak2https://orcid.org/0000-0001-9632-8614Subhadip Pati3https://orcid.org/0000-0002-8878-0915Apratim Dutta4https://orcid.org/0000-0002-9643-5396Saikat Dutta5https://orcid.org/0000-0001-8315-255XSubhanki Dhar6https://orcid.org/0009-0007-2017-5771Tania Sarkar7https://orcid.org/0009-0002-7398-8040Aharna Guin8https://orcid.org/0000-0003-1850-5907Gaurisankar Sa9https://orcid.org/0000-0002-5322-3481Tanya Das10https://orcid.org/0000-0002-9583-0693Division of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaDivision of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata 700054, IndiaCancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs.https://www.explorationpub.com/Journals/ei/Article/1003108antitumor immunitycancer stem cellscancer stem cell sensitizing therapymetastasissuppressive immune cellstumor initiationtumor-microenvironmenttumor relapse |
| spellingShingle | Sourio Chakraborty Sumon Mukherjee Udit Basak Subhadip Pati Apratim Dutta Saikat Dutta Subhanki Dhar Tania Sarkar Aharna Guin Gaurisankar Sa Tanya Das Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy Exploration of Immunology antitumor immunity cancer stem cells cancer stem cell sensitizing therapy metastasis suppressive immune cells tumor initiation tumor-microenvironment tumor relapse |
| title | Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| title_full | Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| title_fullStr | Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| title_full_unstemmed | Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| title_short | Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| title_sort | immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy |
| topic | antitumor immunity cancer stem cells cancer stem cell sensitizing therapy metastasis suppressive immune cells tumor initiation tumor-microenvironment tumor relapse |
| url | https://www.explorationpub.com/Journals/ei/Article/1003108 |
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