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敲低 MSI1 通过使 STAT3 信号失活抑制人口腔鳞状细胞癌的增殖。

Knockdown of MSI1 inhibits the proliferation of human oral squamous cell carcinoma by inactivating STAT3 signaling.

机构信息

Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.

Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu 216000, P.R. China.

出版信息

Int J Mol Med. 2019 Jul;44(1):115-124. doi: 10.3892/ijmm.2019.4181. Epub 2019 May 6.

DOI:10.3892/ijmm.2019.4181
PMID:31059073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6559311/
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.

摘要

肌球蛋白重链结合蛋白 1(MSI1)在多种类型的癌症中高表达;然而,其在口腔鳞状细胞癌(OSCC)中的作用尚不清楚。本研究旨在探讨 MSI1 参与 OSCC 的可能机制。结果表明,MSI1 在 OSCC 组织中上调,而在相邻的正常组织中无表达。MSI1 沉默导致细胞增殖、侵袭和迁移能力下降。此外,MSI1 沉默导致细胞周期在 S 期停滞,下调 c-Myc 和细胞周期蛋白 D1,上调 p21 和 p27 水平。进一步的研究表明,MSI1 抑制抑制信号转导和转录激活因子 3(STAT3)信号的激活。因此,本研究的结果表明,MSI1 沉默可以抑制 OSCC 细胞的增殖和进展,部分通过抑制 c-Myc/STAT3 通路的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/0bed0acce8b5/IJMM-44-01-0115-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/eb9cd50ba925/IJMM-44-01-0115-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/7589232c6ff2/IJMM-44-01-0115-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/625d13c68b82/IJMM-44-01-0115-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/d4978dee0297/IJMM-44-01-0115-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/48051ab5e95a/IJMM-44-01-0115-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/df00fac6197c/IJMM-44-01-0115-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/0bed0acce8b5/IJMM-44-01-0115-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/eb9cd50ba925/IJMM-44-01-0115-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/7589232c6ff2/IJMM-44-01-0115-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/625d13c68b82/IJMM-44-01-0115-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/d4978dee0297/IJMM-44-01-0115-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/48051ab5e95a/IJMM-44-01-0115-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/df00fac6197c/IJMM-44-01-0115-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f76/6559311/0bed0acce8b5/IJMM-44-01-0115-g06.jpg

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