1. Knockdown of MSI1 inhibits the proliferation of human oral squamous cell carcinoma by inactivating STAT3 signaling
- Author
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Xiaomeng Song, Chen‑Fei Wang, Hong‑Chuang Zhang, Xin‑Mei Feng, and Yu‑Nong Wu
- Subjects
0301 basic medicine ,Male ,STAT3 Transcription Factor ,Cell cycle checkpoint ,Cell ,Nerve Tissue Proteins ,Biology ,03 medical and health sciences ,Musashi RNA-binding protein 1 ,0302 clinical medicine ,Cyclin D1 ,Downregulation and upregulation ,Cell Line, Tumor ,Genetics ,medicine ,Gene silencing ,Humans ,STAT3 ,transcription factor ,Cell growth ,RNA-Binding Proteins ,General Medicine ,Articles ,Cell cycle ,Neoplasm Proteins ,oral squamous cell carcinoma ,stomatognathic diseases ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,S Phase Cell Cycle Checkpoints ,Cancer research ,biology.protein ,signal transducer and activator of transcription 3 ,Carcinoma, Squamous Cell ,Female ,Mouth Neoplasms ,Signal Transduction - Abstract
Musashi RNA‑binding protein 1 (MSI1) is highly expressed in several types of cancer; however, its role in oral squamous cell carcinoma (OSCC) remains unknown. The purpose of this study was to investigate the probable mechanism underlying the involvement of MSI1 in OSCC. The results demonstrated that MSI1 was upregulated in OSCC tissues, but not in adjacent healthy tissues. MSI1 silencing resulted in decreased cell proliferative, invasive and migrative capacity. In addition, MSI1 silencing led to cell cycle arrest at the S phase, downregulation of c‑Myc and cyclin D1, and upregulation of p21 and p27 levels. Additional studies demonstrated that MSI1 suppression inhibited the activation of signal transducer and activator of transcription 3 (STAT3) signaling. Accordingly, the findings of the present study suggested that MSI1 silencing can suppress OSCC cell proliferation and progression, in part by inhibiting the activation of the c‑Myc/STAT3 pathway.
- Published
- 2019