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Lentivirus-Mediated Short Hairpin RNA for Follistatin Downregulation Suppresses Tumor Progression in Hypopharyngeal Carcinoma

作     者:Liang GE Shao-feng LIU Liang GE;Shao-feng LIU

作者机构:Department of Otorhinolaryngology Head and Neck Surgerythe Yijishan Hospital of Wannan Medical CollegeWuhu 241001China 

出 版 物:《Current Medical Science》 (当代医学科学(英文))

年 卷 期:2022年第42卷第4期

页      面:832-840页

核心收录:

学科分类:1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100214[医学-肿瘤学] 10[医学] 

基  金:supported by the Project of Young and Middle-aged Scientific Research Fund of Wannan Medical College(No.WK2019F11). 

主  题:follistatin hypopharyngeal carcinoma migration invasion proliferation apoptosis 

摘      要:Objective:Follistatin(FST)inhibits the action of activin by interfering with the binding of activin to its receptor.Although the prognostic value of FST in various cancers has been investigated previously,studies rarely focused on hypopharyngeal carcinoma(HPC).In our study,the effect of FST expression on HPC tissues and cell lines was investigated.Methods:A total of 60 patients with HPC were recruited for this study.Levels of FST mRNA and protein were measured by quantitative polymerase chain reaction(PCR)and immunohistochemistry in HPC tissue samples and by qPCR in the HPC FaDu cells,as well as immortal nasopharyngeal epithelial cell line NP-69 cells.After silencing the FST expression in FaDu cells using lentivirus-mediated siRNA that was specific for FST mRNA,cell proliferation was determined by a Celigo assay.Tumor growth was monitored in nude mice and viability was determined by a methylthiazoletetrazolium assay.The ratio of cell cycle arrest and apoptosis was evaluated by flow cytometry.The colony formation ability was performed using Giemsa staining.In addition,wound healing and Transwell migration and invasion assays were performed for the analysis of cell motility.Results:FST expression was significantly higher in human HPC tissue and FaDu cells than in normal tissue and NP-69 cells.A higher expression of FST in HPC samples was positively correlated with advanced tumors.Moreover,FST knockdown by shRNA significantly decreased cell growth,colony formation,migration and invasion.Furthermore,FST silencing increased the cell apoptosis percentage,and arrested cell cycle in the S phase in FaDu cells.In addition,FST silencing suppressed tumor growth in vivo.Conclusions:Our results indicated that the FST gene was associated with HPC progression and may serve as a potential therapeutic target for the treatment of HPC.

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