EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions
One of the malignant tumors in women that has involved both developed and developing countries is breast cancer. Similar to other types of tumors, breast cancer cells demonstrate high metastatic nature. Besides, breast tumor cells have ability of developing drug resistance. EMT is the related mechan...
| Main Authors: | , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2022-11-01
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| Series: | Biomedicine & Pharmacotherapy |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0753332222011635 |
| _version_ | 1798030975932825600 |
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| author | Mehrdad Hashemi Hamid Zaferani Arani Sima Orouei Shayan Fallah Amin Ghorbani Maryam Khaledabadi Amirabbas Kakavand Alireza Tavakolpournegari Hamidreza Saebfar Hajar Heidari Shokooh Salimimoghadam Maliheh Entezari Afshin Taheriazam Kiavash Hushmandi |
| author_facet | Mehrdad Hashemi Hamid Zaferani Arani Sima Orouei Shayan Fallah Amin Ghorbani Maryam Khaledabadi Amirabbas Kakavand Alireza Tavakolpournegari Hamidreza Saebfar Hajar Heidari Shokooh Salimimoghadam Maliheh Entezari Afshin Taheriazam Kiavash Hushmandi |
| author_sort | Mehrdad Hashemi |
| collection | DOAJ |
| description | One of the malignant tumors in women that has involved both developed and developing countries is breast cancer. Similar to other types of tumors, breast cancer cells demonstrate high metastatic nature. Besides, breast tumor cells have ability of developing drug resistance. EMT is the related mechanism to cancer metastasis and focus of current manuscript is highlighting function of EMT in breast tumor malignancy and drug resistance. Breast tumor cells increase their migration by EMT induction During EMT, N-cadherin and vimentin levels increase, and E-cadherin levels decrease to mediate EMT-induced breast tumor invasion. Different kinds of anti-cancer agents such as tamoxifen, cisplatin and paclitaxel that EMT induction mediates chemoresistance feature of breast tumor cells. Furthermore, EMT induction correlates with radio-resistance in breast tumor. Clinical aspect is reversing EMT in preventing chemotherapy or radiotherapy failure in breast cancer patients and improving their survival time. The anti-tumor agents that suppress EMT can be used for decreasing breast cancer invasion and increasing chemosensitivity of tumor cells. Furthermore, lncRNAs, miRNAs and other factors can modulate EMT in breast tumor progression that are discussed here. |
| first_indexed | 2024-04-11T19:48:52Z |
| format | Article |
| id | doaj.art-1453229c79a74414b4f7b3c7a8fd6e91 |
| institution | Directory Open Access Journal |
| issn | 0753-3322 |
| language | English |
| last_indexed | 2024-04-11T19:48:52Z |
| publishDate | 2022-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Biomedicine & Pharmacotherapy |
| spelling | doaj.art-1453229c79a74414b4f7b3c7a8fd6e912022-12-22T04:06:21ZengElsevierBiomedicine & Pharmacotherapy0753-33222022-11-01155113774EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functionsMehrdad Hashemi0Hamid Zaferani Arani1Sima Orouei2Shayan Fallah3Amin Ghorbani4Maryam Khaledabadi5Amirabbas Kakavand6Alireza Tavakolpournegari7Hamidreza Saebfar8Hajar Heidari9Shokooh Salimimoghadam10Maliheh Entezari11Afshin Taheriazam12Kiavash Hushmandi13Farhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, IranDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Cellular and Molecular Biology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, IranGroup of Mutagenesis, Department of Genetics and Microbiology, Faculty of Biosciences, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, 08193 Barcelona, SpainEuropean University Association, League of European Research Universities, University of Milan, ItalyDepartment of Biomedical Sciences, School of Public Health University at Albany State, University of New York, Albany, NY 12208, USADepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Corresponding authors at: Farhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, IranFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Orthopedics, Faculty of medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Corresponding authors at: Farhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, IranDepartment of Food Hygiene and Quality Control, Division of Epidemiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran; Corresponding author.One of the malignant tumors in women that has involved both developed and developing countries is breast cancer. Similar to other types of tumors, breast cancer cells demonstrate high metastatic nature. Besides, breast tumor cells have ability of developing drug resistance. EMT is the related mechanism to cancer metastasis and focus of current manuscript is highlighting function of EMT in breast tumor malignancy and drug resistance. Breast tumor cells increase their migration by EMT induction During EMT, N-cadherin and vimentin levels increase, and E-cadherin levels decrease to mediate EMT-induced breast tumor invasion. Different kinds of anti-cancer agents such as tamoxifen, cisplatin and paclitaxel that EMT induction mediates chemoresistance feature of breast tumor cells. Furthermore, EMT induction correlates with radio-resistance in breast tumor. Clinical aspect is reversing EMT in preventing chemotherapy or radiotherapy failure in breast cancer patients and improving their survival time. The anti-tumor agents that suppress EMT can be used for decreasing breast cancer invasion and increasing chemosensitivity of tumor cells. Furthermore, lncRNAs, miRNAs and other factors can modulate EMT in breast tumor progression that are discussed here.http://www.sciencedirect.com/science/article/pii/S0753332222011635Breast tumorEMTMetastasisDrug resistanceTumor progression |
| spellingShingle | Mehrdad Hashemi Hamid Zaferani Arani Sima Orouei Shayan Fallah Amin Ghorbani Maryam Khaledabadi Amirabbas Kakavand Alireza Tavakolpournegari Hamidreza Saebfar Hajar Heidari Shokooh Salimimoghadam Maliheh Entezari Afshin Taheriazam Kiavash Hushmandi EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions Biomedicine & Pharmacotherapy Breast tumor EMT Metastasis Drug resistance Tumor progression |
| title | EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions |
| title_full | EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions |
| title_fullStr | EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions |
| title_full_unstemmed | EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions |
| title_short | EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions |
| title_sort | emt mechanism in breast cancer metastasis and drug resistance revisiting molecular interactions and biological functions |
| topic | Breast tumor EMT Metastasis Drug resistance Tumor progression |
| url | http://www.sciencedirect.com/science/article/pii/S0753332222011635 |
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