The dual role of ferroptosis in pancreatic cancer: a narrative review
Abstract. Pancreatic ductal adenocarcinoma is the main cause of cancer-related mortality, with a lack of effective treatments and overall survival rates far lower than other solid cancers. This clinical challenge is related to late diagnosis as well as primary or acquired resistance to therapy-induc...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wolters Kluwer Health/LWW
2021-06-01
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| Series: | Journal of Pancreatology |
| Online Access: | http://journals.lww.com/10.1097/JP9.0000000000000067 |
| _version_ | 1818736913672044544 |
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| author | Daolin Tang Xin Chen Paul B. Comish Rui Kang |
| author_facet | Daolin Tang Xin Chen Paul B. Comish Rui Kang |
| author_sort | Daolin Tang |
| collection | DOAJ |
| description | Abstract. Pancreatic ductal adenocarcinoma is the main cause of cancer-related mortality, with a lack of effective treatments and overall survival rates far lower than other solid cancers. This clinical challenge is related to late diagnosis as well as primary or acquired resistance to therapy-induced apoptosis. Targeting nonapoptotic cell death pathways may provide alternative therapeutic strategies to overcome drug resistance. In particular, recent studies have suggested that ferroptosis, a type of iron-dependent nonapoptotic cell death, is a promising target for pancreatic ductal adenocarcinoma. Ferroptosis can be triggered by inhibiting or activating the redox or iron metabolism-related pathways, mediated by extrinsic/membrane transports (e.g., solute carrier family 7 member 11) or intrinsic/enzymes (e.g., glutathione peroxidase 4). Although the exact effector molecule remains obscure, reactive oxygen species-induced lipid peroxidation and subsequent plasma membrane damage appears to play a central role in mediating ferroptotic death. While treatment-induced ferroptosis is beneficial to suppress tumor growth, inflammation-related immunosuppression caused by ferroptotic damage may promote the occurrence of pancreatic ductal adenocarcinoma. In this review, we outline the latest knowledge about the regulation and function of ferroptosis in pancreatic tumorigenesis and therapy. |
| first_indexed | 2024-12-18T00:44:42Z |
| format | Article |
| id | doaj.art-defbc94b055c498c9a0ff8554ff190d5 |
| institution | Directory Open Access Journal |
| issn | 2096-5664 2577-3577 |
| language | English |
| last_indexed | 2024-12-18T00:44:42Z |
| publishDate | 2021-06-01 |
| publisher | Wolters Kluwer Health/LWW |
| record_format | Article |
| series | Journal of Pancreatology |
| spelling | doaj.art-defbc94b055c498c9a0ff8554ff190d52022-12-21T21:26:47ZengWolters Kluwer Health/LWWJournal of Pancreatology2096-56642577-35772021-06-0142768110.1097/JP9.0000000000000067202106000-00003The dual role of ferroptosis in pancreatic cancer: a narrative reviewDaolin TangXin ChenPaul B. ComishRui KangAbstract. Pancreatic ductal adenocarcinoma is the main cause of cancer-related mortality, with a lack of effective treatments and overall survival rates far lower than other solid cancers. This clinical challenge is related to late diagnosis as well as primary or acquired resistance to therapy-induced apoptosis. Targeting nonapoptotic cell death pathways may provide alternative therapeutic strategies to overcome drug resistance. In particular, recent studies have suggested that ferroptosis, a type of iron-dependent nonapoptotic cell death, is a promising target for pancreatic ductal adenocarcinoma. Ferroptosis can be triggered by inhibiting or activating the redox or iron metabolism-related pathways, mediated by extrinsic/membrane transports (e.g., solute carrier family 7 member 11) or intrinsic/enzymes (e.g., glutathione peroxidase 4). Although the exact effector molecule remains obscure, reactive oxygen species-induced lipid peroxidation and subsequent plasma membrane damage appears to play a central role in mediating ferroptotic death. While treatment-induced ferroptosis is beneficial to suppress tumor growth, inflammation-related immunosuppression caused by ferroptotic damage may promote the occurrence of pancreatic ductal adenocarcinoma. In this review, we outline the latest knowledge about the regulation and function of ferroptosis in pancreatic tumorigenesis and therapy.http://journals.lww.com/10.1097/JP9.0000000000000067 |
| spellingShingle | Daolin Tang Xin Chen Paul B. Comish Rui Kang The dual role of ferroptosis in pancreatic cancer: a narrative review Journal of Pancreatology |
| title | The dual role of ferroptosis in pancreatic cancer: a narrative review |
| title_full | The dual role of ferroptosis in pancreatic cancer: a narrative review |
| title_fullStr | The dual role of ferroptosis in pancreatic cancer: a narrative review |
| title_full_unstemmed | The dual role of ferroptosis in pancreatic cancer: a narrative review |
| title_short | The dual role of ferroptosis in pancreatic cancer: a narrative review |
| title_sort | dual role of ferroptosis in pancreatic cancer a narrative review |
| url | http://journals.lww.com/10.1097/JP9.0000000000000067 |
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