Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future
Pancreatic cancer (PC) is a devastating malignant tumor of gastrointestinal (GI) tumors characterized by late diagnosis, low treatment success and poor prognosis. The most common pathological type of PC is pancreatic ductal adenocarcinoma (PDAC), which accounts for approximately 95% of PC. PDAC is p...
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| Format: | Article |
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MDPI AG
2022-11-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/23/15031 |
| _version_ | 1797463114213490688 |
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| author | Chang Li Xunzhe Yin Zuojia Liu Jin Wang |
| author_facet | Chang Li Xunzhe Yin Zuojia Liu Jin Wang |
| author_sort | Chang Li |
| collection | DOAJ |
| description | Pancreatic cancer (PC) is a devastating malignant tumor of gastrointestinal (GI) tumors characterized by late diagnosis, low treatment success and poor prognosis. The most common pathological type of PC is pancreatic ductal adenocarcinoma (PDAC), which accounts for approximately 95% of PC. PDAC is primarily driven by the Kirsten rat sarcoma virus (KRAS) oncogene. Ferroptosis was originally described as ras-dependent cell death but is now defined as a regulated cell death caused by iron accumulation and lipid peroxidation. Recent studies have revealed that ferroptosis plays an important role in the development and therapeutic response of tumors, especially PDAC. As the non-apoptotic cell death, ferroptosis may minimize the emergence of drug resistance for clinical trials of PDAC. This article reviews what has been learned in recent years about the mechanisms of ferroptosis in PDAC, introduces the association between ferroptosis and the KRAS target, and summarizes several potential strategies that are capable of triggering ferroptosis to suppress PDAC progression. |
| first_indexed | 2024-03-09T17:46:03Z |
| format | Article |
| id | doaj.art-fb0be317e6c94b818636374d70035fb1 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T17:46:03Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-fb0be317e6c94b818636374d70035fb12023-11-24T11:12:03ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-11-0123231503110.3390/ijms232315031Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising FutureChang Li0Xunzhe Yin1Zuojia Liu2Jin Wang3State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, ChinaState Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, ChinaState Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, ChinaDepartment of Chemistry and Physics, Stony Brook University, Stony Brook, NY 11794-3400, USAPancreatic cancer (PC) is a devastating malignant tumor of gastrointestinal (GI) tumors characterized by late diagnosis, low treatment success and poor prognosis. The most common pathological type of PC is pancreatic ductal adenocarcinoma (PDAC), which accounts for approximately 95% of PC. PDAC is primarily driven by the Kirsten rat sarcoma virus (KRAS) oncogene. Ferroptosis was originally described as ras-dependent cell death but is now defined as a regulated cell death caused by iron accumulation and lipid peroxidation. Recent studies have revealed that ferroptosis plays an important role in the development and therapeutic response of tumors, especially PDAC. As the non-apoptotic cell death, ferroptosis may minimize the emergence of drug resistance for clinical trials of PDAC. This article reviews what has been learned in recent years about the mechanisms of ferroptosis in PDAC, introduces the association between ferroptosis and the KRAS target, and summarizes several potential strategies that are capable of triggering ferroptosis to suppress PDAC progression.https://www.mdpi.com/1422-0067/23/23/15031ferroptosisPDACKRAStumorigenesistherapy |
| spellingShingle | Chang Li Xunzhe Yin Zuojia Liu Jin Wang Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future International Journal of Molecular Sciences ferroptosis PDAC KRAS tumorigenesis therapy |
| title | Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future |
| title_full | Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future |
| title_fullStr | Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future |
| title_full_unstemmed | Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future |
| title_short | Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future |
| title_sort | emerging potential mechanism and therapeutic target of ferroptosis in pdac a promising future |
| topic | ferroptosis PDAC KRAS tumorigenesis therapy |
| url | https://www.mdpi.com/1422-0067/23/23/15031 |
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