A Combination of EGFR Inhibitors and AE-PDT Could Synergistically Suppress Breast Cancer Progression
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
BACKGROUND: Breast cancer is the most frequently diagnosed malignancy and the leading cause of cancerrelated deaths in women. Activation of EGFR by EC-secreted EGFR ligands promotes breast cancer progression. Current treatments provide limited benefits in triple-negative breast cancer (TNBC). Photodynamic therapy (PDT) has been proven effective for the treatment of TNBC through the EGFR pathway, but the underlying mechanism is still unclear.
PURPOSE: The purpose of this study was to determine the role of the EGFR pathway in the treatment of PDT on TNBC in a co-culture system.
METHODS: MB-231 and HUVEC were co-cultured for experiments (HU-231). Cell viability and ROS production were detected after AE-PDT, a combination of EGFR inhibitors (AEE788)with PDT to test angiogenesis, apoptosis, and pyroptosis. WB detects expression of EGFR. EGFR, P-EGFR, VEGF, caspase-1, capase-3, and GSDMD.
RESULTS: AE-PDT inhibited HU-231 cell proliferation and tumor angiogenesis, and induced cell apoptosis and pyroptosis by promoting ROS production. AEE788, an inhibitor of the EGFR, enhanced HU-231 cell killing after AE-PDT.
CONCLUSION: Our study suggested that the combination of EGFR inhibitors and AE-PDT could synergistically suppress breast cancer progression, providing a new treatment strategy.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:23 |
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| Enthalten in: |
Anti-cancer agents in medicinal chemistry - 23(2023), 19 vom: 21., Seite 2135-2145 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Niu, Yajuan [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 23.11.2023 Date Revised 21.02.2024 published: Print Citation Status MEDLINE |
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| doi: |
10.2174/1871520623666230908145748 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
| 520 | |a BACKGROUND: Breast cancer is the most frequently diagnosed malignancy and the leading cause of cancerrelated deaths in women. Activation of EGFR by EC-secreted EGFR ligands promotes breast cancer progression. Current treatments provide limited benefits in triple-negative breast cancer (TNBC). Photodynamic therapy (PDT) has been proven effective for the treatment of TNBC through the EGFR pathway, but the underlying mechanism is still unclear | ||
| 520 | |a PURPOSE: The purpose of this study was to determine the role of the EGFR pathway in the treatment of PDT on TNBC in a co-culture system | ||
| 520 | |a METHODS: MB-231 and HUVEC were co-cultured for experiments (HU-231). Cell viability and ROS production were detected after AE-PDT, a combination of EGFR inhibitors (AEE788)with PDT to test angiogenesis, apoptosis, and pyroptosis. WB detects expression of EGFR. EGFR, P-EGFR, VEGF, caspase-1, capase-3, and GSDMD | ||
| 520 | |a RESULTS: AE-PDT inhibited HU-231 cell proliferation and tumor angiogenesis, and induced cell apoptosis and pyroptosis by promoting ROS production. AEE788, an inhibitor of the EGFR, enhanced HU-231 cell killing after AE-PDT | ||
| 520 | |a CONCLUSION: Our study suggested that the combination of EGFR inhibitors and AE-PDT could synergistically suppress breast cancer progression, providing a new treatment strategy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a EGFR pathway | |
| 650 | 4 | |a angiogenesis | |
| 650 | 4 | |a apoptosis | |
| 650 | 4 | |a breast cancer. | |
| 650 | 4 | |a photodynamic therapy (PDT) | |
| 650 | 4 | |a pyroptosis | |
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| 700 | 1 | |a Guo, Xiya |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Wang |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Xiaoyu |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Kaiting |e verfasserin |4 aut | |
| 700 | 1 | |a Tian, Si |e verfasserin |4 aut | |
| 700 | 1 | |a Zhu, Ying |e verfasserin |4 aut | |
| 700 | 1 | |a Bai, DingQun |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Qing |e verfasserin |4 aut | |
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