MicroRNA-125b exerts antitumor functions in cutaneous squamous cell carcinoma by targeting the STAT3 pathway
Autor: | Wanggen Liu, Guoying Miao, Chunxia Yao, Jing Zhang, Jingyuan Liu, Nan Zhao, Ke Tian, Xiaoyi Fan |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
STAT3 Transcription Factor
Skin Neoplasms Apoptosis Biochemistry Flow cytometry Cyclin D1 Downregulation and upregulation Cell Line Tumor medicine Research Letter Humans MTT assay lcsh:QH573-671 STAT3 Molecular Biology Signal transducer and activator of transcription (STAT) 3 Cell Proliferation medicine.diagnostic_test biology Cell growth Chemistry lcsh:Cytology microRNA-125b Cell Biology Cutaneous squamous cell carcinoma Molecular medicine Gene Expression Regulation Neoplastic MicroRNAs Proto-Oncogene Proteins c-bcl-2 Cancer research STAT protein biology.protein Carcinoma Squamous Cell Signal Transduction |
Zdroj: | Cellular & Molecular Biology Letters, Vol 25, Iss 1, Pp 1-12 (2020) Cellular & Molecular Biology Letters |
ISSN: | 1689-1392 1425-8153 |
DOI: | 10.1186/s11658-020-00207-y |
Popis: | Background MicroRNA-125b (miR-125b) is downregulated in human cutaneous squamous cell carcinoma (CSCC). However, its function in CSCC has yet to be extensively explored. Here, we analyze the relationship between signal transducer and activator of transcription 3 (STAT3) and miR-125b in CSCC. Methods Western blotting and quantitative RT-PCR were used to determine the expression of the miR-125b–STAT3 axis in human CSCC tissues and cell lines. The direct regulatory effect of miR-125b on STAT3 expression was assessed using a luciferase reporter gene assay and RNA immunoprecipitation assay. The MTT assay and flow cytometry were used to determine the role of the miR-125b–STAT3 axis in CSCC cell proliferation and apoptosis. Results MiR-125b expression levels were significantly lower in CSCC cell lines and tissues than in normal cell lines and tissues. STAT3 was identified as the direct target of miR-125b. Upregulation of miR-125b and downregulation of STAT3 suppressed cell proliferation and promoted cell apoptosis. Cyclin D1 and Bcl2 were identified as the downstream targets of the miR-125–STAT3 axis. Conclusions Our findings indicate that miR-125b acts as a tumor suppressor in CSCC by targeting the STAT3 pathway. This observation increases our understanding of the molecular mechanisms of CSCC. Therapies aimed at activating miR-125b or inhibiting STAT3 signaling should be explored as potential treatments for CSCC. |
Databáze: | OpenAIRE |
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