文献类型：期刊文献

英文题名：Extracellular Vesicle-Derived miR-105-5p Promotes Malignant Phenotypes of Esophageal Squamous Cell Carcinoma by Targeting SPARCL1 via FAK/AKT Signaling Pathway

作者：He, Binjun[1,2];Zhang, Kang[2];Han, Xiaoliang[2];Su, Chao[2];Zhao, Jiaming[2];Wang, Guoxia[2];Wang, Guzong[2];Zhang, Liuya[2];Hu, Wenbin[2]

机构：[1]Zhejiang Univ, Shaoxing Peoples Hosp, Sch Med, Dept Thorac Surg, Shaoxing, Peoples R China;[2]Shaoxing Univ, Affiliated Hosp, Shaoxing Municipal Hosp, Dept Thorac Surg, Shaoxing, Peoples R China

年份：2022

卷号：13

外文期刊名：FRONTIERS IN GENETICS

收录：SCI-EXPANDED(收录号：WOS:000772145400001)、、Scopus(收录号：2-s2.0-85126752241)、WOS

基金：Funding This study was funded by the Shaoxing Science and Technology Project (No. 2020A13059).

语种：英文

外文关键词：EVs; miR-105-5p; SPARCL1; ESCC; FAK; AKT; proliferation; migration; invasion

外文摘要：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.