Extracellular Vesicle-Derived miR-105-5p Promotes Malignant Phenotypes of Esophageal Squamous Cell Carcinoma by Targeting SPARCL1 via FAK/AKT Signaling Pathway
Copyright © 2022 He, Zhang, Han, Su, Zhao, Wang, Wang, Zhang and Hu..
Objective: Esophageal squamous cell carcinoma (ESCC) presents high morbidity and mortality. It was demonstrated that blood-derived vesicles can facilitate ESCC development and transmit regulating signals. However, the molecular mechanism of vesicle miRNA secreted by tumor cells affecting ESCC progression has not been explored. Methods: The mRNA-related signaling pathways and differentially expressed genes were screened out in TCGA dataset. The levels of miRNA-105-5p and SPARCL1 were determined by qRT-PCR. Protein level determination was processed using Western blot. The interaction between the two genes was verified with the dual-luciferase method. A transmission electron microscope was utilized to further identify extracellular vesicles (EVs), and co-culture assay was performed to validate the intake of EVs. In vitro experiments were conducted to evaluate cell function changes in ESCC. A mice tumor formation experiment was carried out to observe tumor growth in vivo. Results: MiRNA-105-5p expression was increased in ESCC, while SPARCL1 was less expressed. MiRNA-105-5p facilitated cell behaviors in ESCC through targeting SPARCL1 and regulating the focal adhesion kinase (FAK)/Akt signaling pathway. Blood-derived external vesicles containing miRNA-105-5p and EVs could be internalized by ESCC cells. Then, miRNA-105-5p could be transferred to ESCC cells to foster tumorigenesis as well as cell behaviors. Conclusion: EV-carried miRNA-105-5p entered ESCC cells and promoted tumor-relevant functions by mediating SPARCL1 and the FAK/Akt signaling pathway, which indicated that the treatment of ESCC via serum EVs might be a novel therapy and that miRNA-105-5p can be a molecular target for ESCC therapy.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:13 |
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| Enthalten in: |
Frontiers in genetics - 13(2022) vom: 17., Seite 819699 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
He, Binjun [VerfasserIn] |
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| Links: |
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| Themen: |
ESCC |
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| Anmerkungen: |
Date Revised 22.03.2022 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| doi: |
10.3389/fgene.2022.819699 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM338396373 |
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| 245 | 1 | 0 | |a Extracellular Vesicle-Derived miR-105-5p Promotes Malignant Phenotypes of Esophageal Squamous Cell Carcinoma by Targeting SPARCL1 via FAK/AKT Signaling Pathway |
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| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a Copyright © 2022 He, Zhang, Han, Su, Zhao, Wang, Wang, Zhang and Hu. | ||
| 520 | |a Objective: Esophageal squamous cell carcinoma (ESCC) presents high morbidity and mortality. It was demonstrated that blood-derived vesicles can facilitate ESCC development and transmit regulating signals. However, the molecular mechanism of vesicle miRNA secreted by tumor cells affecting ESCC progression has not been explored. Methods: The mRNA-related signaling pathways and differentially expressed genes were screened out in TCGA dataset. The levels of miRNA-105-5p and SPARCL1 were determined by qRT-PCR. Protein level determination was processed using Western blot. The interaction between the two genes was verified with the dual-luciferase method. A transmission electron microscope was utilized to further identify extracellular vesicles (EVs), and co-culture assay was performed to validate the intake of EVs. In vitro experiments were conducted to evaluate cell function changes in ESCC. A mice tumor formation experiment was carried out to observe tumor growth in vivo. Results: MiRNA-105-5p expression was increased in ESCC, while SPARCL1 was less expressed. MiRNA-105-5p facilitated cell behaviors in ESCC through targeting SPARCL1 and regulating the focal adhesion kinase (FAK)/Akt signaling pathway. Blood-derived external vesicles containing miRNA-105-5p and EVs could be internalized by ESCC cells. Then, miRNA-105-5p could be transferred to ESCC cells to foster tumorigenesis as well as cell behaviors. Conclusion: EV-carried miRNA-105-5p entered ESCC cells and promoted tumor-relevant functions by mediating SPARCL1 and the FAK/Akt signaling pathway, which indicated that the treatment of ESCC via serum EVs might be a novel therapy and that miRNA-105-5p can be a molecular target for ESCC therapy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a ESCC | |
| 650 | 4 | |a EVs | |
| 650 | 4 | |a FAK/AKT | |
| 650 | 4 | |a SPARCL1 | |
| 650 | 4 | |a invasion | |
| 650 | 4 | |a miR-105-5p | |
| 650 | 4 | |a migration | |
| 650 | 4 | |a proliferation | |
| 700 | 1 | |a Zhang, Kang |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Xiaoliang |e verfasserin |4 aut | |
| 700 | 1 | |a Su, Chao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Jiaming |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Guoxia |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Guzong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Liuya |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Wenbin |e verfasserin |4 aut | |
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