Oncotarget

Research Papers:

LncRNA LOC653786 promotes growth of RCC cells via upregulating FOXM1

Fan Yang, Qingjian Wu, Yan Zhang, Haojun Xiong, Xinzhe Li, Bo Li, Wei Xie, Le Zhang, Min Xu, Kebin Zhang and Fengtian He _

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Oncotarget. 2018; 9:12101-12111. https://doi.org/10.18632/oncotarget.24027

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Abstract

Fan Yang1,2,*, Qingjian Wu3,*, Yan Zhang1, Haojun Xiong1, Xinzhe Li1, Bo Li1, Wei Xie2, Le Zhang2, Min Xu4, Kebin Zhang2 and Fengtian He1

1Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China

2Central Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China

3Department of Urology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China

4Center for Disease Control and Prevention, Chengdu Military Region, Chengdu 610021, China

*These authors have contributed equally to this work

Correspondence to:

Fengtian He, email: hefengtian66@163.com

Kebin Zhang, email: zhangkebin12@163.com

Min Xu, email: 603537726@qq.com

Keywords: LOC653786; FOXM1; long noncoding RNA; renal cell carcinoma; cell growth

Received: August 02, 2017     Accepted: January 02, 2018     Published: January 08, 2018

ABSTRACT

Renal cell carcinoma (RCC) is the most common kidney malignancy with poor prognosis. Recently, long noncoding RNAs (lncRNAs) have been demonstrated as important regulators in multiple cancers including RCC. LOC653786 is a lncRNA, but its role in cancer remains unclear. In this study, we for the first time found that LOC653786 was upregulated in RCC tissues and cell lines, and this lncRNA promoted growth and cell cycle progression of RCC cells. Moreover, we showed that LOC653786 elevated the expression of forkhead box M1 (FOXM1) and its downstream target genes cyclin D1 and cyclin B1 in RCC cells. Reporter assay revealed that LOC653786 enhanced the transcriptional activity of FOXM1 gene promoter. Additionally, knockdown of FOXM1 attenuated the LOC653786-enhanced growth and cell cycle progression of RCC cells. Meanwhile, silencing of LOC653786 suppressed RCC cell growth and cell cycle progression, which was alleviated by overexpression of FOXM1. The in vivo experiments in nude mice showed knockdown of LOC653786 repressed xenograft tumor growth and FOXM1 expression. In conclusion, our results demonstrate that LOC653786 accelerates growth and cell cycle progression of RCC cells via upregulating FOXM1, suggesting that the ‘LOC653786/FOXM1’ pathway may serve as a novel target for RCC treatment.


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