ArticleCurrent medical science2022
Lentivirus-Mediated Short Hairpin RNA for Follistatin Downregulation Suppresses Tumor Progression in Hypopharyngeal Carcinoma.
Article in Current medical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
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2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveFollistatin (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.
methodsA 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.
resultsFST 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.
conclusionsOur 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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