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KLF8基因敲低抑制人骨肉瘤细胞的增殖和侵袭。

KLF8 knockdown suppresses proliferation and invasion in human osteosarcoma cells.

作者信息

Lin Feng, Shen Zan, Tang Li-Na, Zheng Shui-Er, Sun Yuan-Jue, Min Da-Liu, Yao Yang

机构信息

Graduate School of Medicine, Soochow University, Suzhou, Jiangsu 215006, P.R. China.

Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.

出版信息

Mol Med Rep. 2014 May;9(5):1613-7. doi: 10.3892/mmr.2014.2027. Epub 2014 Mar 7.

DOI:10.3892/mmr.2014.2027
PMID:24604387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4020472/
Abstract

Krüppel-like factor 8 (KLF8) is a transcription factor that is important in the regulation of the cell cycle and has a critical role in oncogenic transformation and epithelial to mesenchymal transition (EMT). EMT is a key process in tumor metastasis. Although overexpression of KLF8 has been observed in a variety of human tumor types, the role of KLF8 in human osteosarcoma is yet to be elucidated. The present study aimed to investigate the biological impact of KLF8 on Saos-2 osteosarcoma cells. KLF8 gene expression was knocked down in vitro using a lentivirus-mediated small interfering (si)RNA method. Cell proliferation and cell cycle distribution were evaluated using 3-(4,5)-dimethylthiahiazo(-z-yl)-3,5-di-phenytetrazoliumromide and colony formation assays, and flow cytometry, respectively. Cell invasion was analyzed using a Transwell® invasion assay. Knockdown of KLF8 was found to significantly inhibit proliferation and invasion in osteosarcoma cells. These data suggest that KLF8 may exhibit an important role in osteosarcoma tumorigenesis and that KLF8 may be a potential therapeutic target for the treatment of osteosarcoma.

摘要

Krüppel样因子8（KLF8）是一种转录因子，在细胞周期调控中起重要作用，在致癌转化和上皮-间质转化（EMT）中起关键作用。EMT是肿瘤转移中的一个关键过程。尽管在多种人类肿瘤类型中均观察到KLF8的过表达，但KLF8在人类骨肉瘤中的作用尚待阐明。本研究旨在探讨KLF8对Saos-2骨肉瘤细胞的生物学影响。采用慢病毒介导的小干扰（si）RNA方法在体外敲低KLF8基因表达。分别使用3-（4,5）-二甲基噻唑（-z-基）-3,5-二苯基四氮唑溴盐和集落形成试验以及流式细胞术评估细胞增殖和细胞周期分布。使用Transwell®侵袭试验分析细胞侵袭。发现敲低KLF8可显著抑制骨肉瘤细胞的增殖和侵袭。这些数据表明，KLF8可能在骨肉瘤肿瘤发生中发挥重要作用，并且KLF8可能是治疗骨肉瘤的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/c26ea4627be0/MMR-09-05-1613-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/e6e9bed3cf4d/MMR-09-05-1613-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/ede9bd0fdbef/MMR-09-05-1613-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/b0af5cc8d878/MMR-09-05-1613-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/c26ea4627be0/MMR-09-05-1613-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/e6e9bed3cf4d/MMR-09-05-1613-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/ede9bd0fdbef/MMR-09-05-1613-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/b0af5cc8d878/MMR-09-05-1613-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/4020472/c26ea4627be0/MMR-09-05-1613-g03.jpg

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A novel role of Krüppel-like factor 8 in DNA repair in breast cancer cells.
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miR-24-3p/KLF8 Signaling Axis Contributes to LUAD Metastasis by Regulating EMT.miR-24-3p/KLF8 信号轴通过调控 EMT 促进 LUAD 转移。
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