ER stress and/or ER-phagy in drug resistance? Three coincidences are proof
Abstract Cancer is influenced by the tumor microenvironment (TME), which includes factors such as pH, hypoxia, immune cells, and blood vessels. These factors affect cancer cell growth and behavior. The tumor microenvironment triggers adaptive responses such as endoplasmic reticulum (ER) stress, unfo...
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| Format: | Article |
| Language: | English |
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BMC
2025-05-01
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| Series: | Cell Communication and Signaling |
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| Online Access: | https://doi.org/10.1186/s12964-025-02232-w |
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| author | Sameer Kumar Panda Ibone Rubio Sanchez-Pajares Ayesha Rehman Vitale Del Vecchio Luigi Mele Sandhya Chipurupalli Nirmal Robinson Vincenzo Desiderio |
| author_facet | Sameer Kumar Panda Ibone Rubio Sanchez-Pajares Ayesha Rehman Vitale Del Vecchio Luigi Mele Sandhya Chipurupalli Nirmal Robinson Vincenzo Desiderio |
| author_sort | Sameer Kumar Panda |
| collection | DOAJ |
| description | Abstract Cancer is influenced by the tumor microenvironment (TME), which includes factors such as pH, hypoxia, immune cells, and blood vessels. These factors affect cancer cell growth and behavior. The tumor microenvironment triggers adaptive responses such as endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and autophagy, posing a challenge to cancer treatment. The UPR aims to restore ER homeostasis by involving key regulators inositol-requiring enzyme-1(IRE1), PKR-like ER kinase (PERK), and activating transcription factor 6 (ATF6). Additionally, ER-phagy, a selective form of autophagy, eliminates ER components under stress conditions. Understanding the interplay between hypoxia, ER stress, UPR, and autophagy in the tumor microenvironment is crucial for developing effective cancer therapies to overcome drug resistance. Targeting the components of the UPR and modulating ER-phagy could potentially improve the efficacy of existing cancer therapies. Future research should define the conditions under which ER stress responses and ER-phagy act as pro-survival versus pro-death mechanisms and develop precise methods to quantify ER-phagic flux in tumor cells. |
| format | Article |
| id | doaj-art-ef2fa2d71a7540be8bc22be3d398a85f |
| institution | Kabale University |
| issn | 1478-811X |
| language | English |
| publishDate | 2025-05-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell Communication and Signaling |
| spelling | doaj-art-ef2fa2d71a7540be8bc22be3d398a85f2025-08-20T03:53:58ZengBMCCell Communication and Signaling1478-811X2025-05-0123111410.1186/s12964-025-02232-wER stress and/or ER-phagy in drug resistance? Three coincidences are proofSameer Kumar Panda0Ibone Rubio Sanchez-Pajares1Ayesha Rehman2Vitale Del Vecchio3Luigi Mele4Sandhya Chipurupalli5Nirmal Robinson6Vincenzo Desiderio7Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”University of BasilicataCenter for Cancer Biology, University of South Australia and SA PathologyCenter for Cancer Biology, University of South Australia and SA PathologyDepartment of Experimental Medicine, University of Campania “Luigi Vanvitelli”Abstract Cancer is influenced by the tumor microenvironment (TME), which includes factors such as pH, hypoxia, immune cells, and blood vessels. These factors affect cancer cell growth and behavior. The tumor microenvironment triggers adaptive responses such as endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and autophagy, posing a challenge to cancer treatment. The UPR aims to restore ER homeostasis by involving key regulators inositol-requiring enzyme-1(IRE1), PKR-like ER kinase (PERK), and activating transcription factor 6 (ATF6). Additionally, ER-phagy, a selective form of autophagy, eliminates ER components under stress conditions. Understanding the interplay between hypoxia, ER stress, UPR, and autophagy in the tumor microenvironment is crucial for developing effective cancer therapies to overcome drug resistance. Targeting the components of the UPR and modulating ER-phagy could potentially improve the efficacy of existing cancer therapies. Future research should define the conditions under which ER stress responses and ER-phagy act as pro-survival versus pro-death mechanisms and develop precise methods to quantify ER-phagic flux in tumor cells.https://doi.org/10.1186/s12964-025-02232-wER StressUPRER-phagyAutophagyDrug resistance |
| spellingShingle | Sameer Kumar Panda Ibone Rubio Sanchez-Pajares Ayesha Rehman Vitale Del Vecchio Luigi Mele Sandhya Chipurupalli Nirmal Robinson Vincenzo Desiderio ER stress and/or ER-phagy in drug resistance? Three coincidences are proof Cell Communication and Signaling ER Stress UPR ER-phagy Autophagy Drug resistance |
| title | ER stress and/or ER-phagy in drug resistance? Three coincidences are proof |
| title_full | ER stress and/or ER-phagy in drug resistance? Three coincidences are proof |
| title_fullStr | ER stress and/or ER-phagy in drug resistance? Three coincidences are proof |
| title_full_unstemmed | ER stress and/or ER-phagy in drug resistance? Three coincidences are proof |
| title_short | ER stress and/or ER-phagy in drug resistance? Three coincidences are proof |
| title_sort | er stress and or er phagy in drug resistance three coincidences are proof |
| topic | ER Stress UPR ER-phagy Autophagy Drug resistance |
| url | https://doi.org/10.1186/s12964-025-02232-w |
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