Anticancer effects of miR-124 delivered by BM-MSC derived exosomes on cell proliferation, epithelial mesenchymal transition, and chemotherapy sensitivity of pancreatic cancer cells
OBJECTIVE: This study aims to explore the roles of miR-124 in pancreatic tumor and potential vehicles.
RESULTS: The miR-124 expression levels decreased in pancreatic adenocarcinoma tissues and cancer cell lines AsPC-1, PANC1, BxPC-3 and SW1990. Furthermore, the elevated expression of miR-124 in AsPC-1 and PANC1 via miR-124 mimic transfection-induced apoptosis, metastasis and epithelial mesenchymal transition was suppressed, and the EZH2 overexpression partly reversed the protective effects of miR-124 against pancreatic tumors. In addition, the expression of miR-124 was detected in exosomes extracted from miR-124-transfected BM-MSCs, and these exosomes delivered miR-124 into pancreatic cancer cells, and presented the anti-tumor effects in vitro and in vivo.
CONCLUSION: MiR-124-carried BM-MSC-derived exosomes have potential applications for the treatment of pancreatic tumors.
METHODS: The expression of miR-124 and EZH2 was determined in both pancreatic cancer tissues and cell lines. miR-124 or EZH2 was overexpressed in AsPC-1 and PANC1 cells. Then, the effects on cell viability. apoptosis, invasion, migration and epithelial mesenchymal transition were evaluated. Afterwards, the roles of miR-124 on the expression and function of EZH2 in pancreatic tumors were determined by dual luciferase reporter assay. Subsequently, miR-124 was transfected to bone marrow mesenchymal stromal cells (BM-MSCs), and the BM-MSCs derived exosomes were isolated and co-cultured with AsPC-1 and PANC1 cells, or injected into pancreatic cancer tumor-bearing mice.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:12 |
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Enthalten in: |
Aging - 12(2020), 19 vom: 11. Okt., Seite 19660-19676 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Xu, Yan [VerfasserIn] |
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Links: |
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Themen: |
BM-MSCs |
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Anmerkungen: |
Date Revised 23.01.2023 published: Print-Electronic Citation Status PubMed-not-MEDLINE |
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doi: |
10.18632/aging.103997 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM316099449 |
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500 | |a published: Print-Electronic | ||
500 | |a Citation Status PubMed-not-MEDLINE | ||
520 | |a OBJECTIVE: This study aims to explore the roles of miR-124 in pancreatic tumor and potential vehicles | ||
520 | |a RESULTS: The miR-124 expression levels decreased in pancreatic adenocarcinoma tissues and cancer cell lines AsPC-1, PANC1, BxPC-3 and SW1990. Furthermore, the elevated expression of miR-124 in AsPC-1 and PANC1 via miR-124 mimic transfection-induced apoptosis, metastasis and epithelial mesenchymal transition was suppressed, and the EZH2 overexpression partly reversed the protective effects of miR-124 against pancreatic tumors. In addition, the expression of miR-124 was detected in exosomes extracted from miR-124-transfected BM-MSCs, and these exosomes delivered miR-124 into pancreatic cancer cells, and presented the anti-tumor effects in vitro and in vivo | ||
520 | |a CONCLUSION: MiR-124-carried BM-MSC-derived exosomes have potential applications for the treatment of pancreatic tumors | ||
520 | |a METHODS: The expression of miR-124 and EZH2 was determined in both pancreatic cancer tissues and cell lines. miR-124 or EZH2 was overexpressed in AsPC-1 and PANC1 cells. Then, the effects on cell viability. apoptosis, invasion, migration and epithelial mesenchymal transition were evaluated. Afterwards, the roles of miR-124 on the expression and function of EZH2 in pancreatic tumors were determined by dual luciferase reporter assay. Subsequently, miR-124 was transfected to bone marrow mesenchymal stromal cells (BM-MSCs), and the BM-MSCs derived exosomes were isolated and co-cultured with AsPC-1 and PANC1 cells, or injected into pancreatic cancer tumor-bearing mice | ||
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700 | 1 | |a Zhou, Deren |e verfasserin |4 aut | |
700 | 1 | |a Lin, Rui |e verfasserin |4 aut | |
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700 | 1 | |a Shi, Baomin |e verfasserin |4 aut | |
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