Searching for just a few words should be enough to get started. If you need to make more complex queries, use the tips below to guide you.
Article type: Research Article
Authors: Zhu, Lina; 1 | Chen, Yinana; 1 | Liu, Jingb | Nie, Kaic | Xiao, Yongxinc | Yu, Honga; *
Affiliations: [a] Department of Radiology, Shanghai Chest Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China | [b] Department of Radiology, Dongfang Hospital Affiliated to Shanghai Tongji University, Shanghai, China | [c] Department of Radiology, Shanghai Changzheng Hospital Affiliated to the Second Military Medical University, Shanghai, China
Correspondence: [*] Corresponding author: Hong Yu, Department of Radiology, Shanghai Chest Hospital Affiliated to Shanghai Jiaotong University, No. 241 Huaihai West Road, Xuhui District, Shanghai 200030, China. Tel.: +86 21 38804518; E-mail: [email protected].
Note: [1] Lin Zhu and Yinan Chen contributed equally to this work.
Abstract: OBJECTIVE: MicroRNA-629 (miR-629) has been found to play an important role in the pathogenesis of human cancers. However, the function of miR-629 is still unknown in non-small-cell lung cancer (NSCLC). The purpose of this study is to preliminarily elucidate the regulatory mechanism of miR-629 in NSCLC. MATERIALS AND METHODS: The mRNA and protein expression was measured by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. The function of miR-629 was investigated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and Transwell assays. The relationship between miR-629 and FOXO1 was confirmed by dual luciferase assay. RESULTS: MiR-629 was upregulated in NSCLC tissues and cells. High expression of miR-629 predicted poor prognosis in patients with NSCLC. Moreover, miR-629 promoted cell proliferation, migration and invasion in NSCLC cells. In addition, FOXO1 was confirmed as a direct target of miR-629 in NSCLC. Furthermore, knockdown of FOXO1 also promoted proliferation, migration and invasion of NSCLC cells. More importantly, overexpression of FOXO1 weakened the carcinogenesis of miR-629 in NSCLC. Besides that, miR-629 promoted EMT and activated the PI3K/AKT pathway in NSCLC. CONCLUSIONS: MiR-629 promotes the progression of NSCLC by targeting FOXO1 and regulating EMT/PI3K/AKT pathway.
Keywords: miR-629, non-small-cell lung cancer, FOXO1, PI3K/AKT pathway
DOI: 10.3233/CBM-201685
Journal: Cancer Biomarkers, vol. 29, no. 3, pp. 347-357, 2020
IOS Press, Inc.
6751 Tepper Drive
Clifton, VA 20124
USA
Tel: +1 703 830 6300
Fax: +1 703 830 2300
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
IOS Press
Nieuwe Hemweg 6B
1013 BG Amsterdam
The Netherlands
Tel: +31 20 688 3355
Fax: +31 20 687 0091
[email protected]
For editorial issues, permissions, book requests, submissions and proceedings, contact the Amsterdam office [email protected]
Inspirees International (China Office)
Ciyunsi Beili 207(CapitaLand), Bld 1, 7-901
100025, Beijing
China
Free service line: 400 661 8717
Fax: +86 10 8446 7947
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
如果您在出版方面需要帮助或有任何建, 件至: [email protected]