Research Papers: Gerotarget (Focus on Aging):

Identification of the lncRNA, AK156230, as a novel regulator of cellular senescence in mouse embryonic fibroblasts

Yu-ning Chen, Meng-yun Cai, Shun Xu, Mei Meng, ingcong Ren, Jay W. Yang, Yu-qi Dong, Xinguang Liu, Jin-Ming Yang and Xing-dong Xiong _

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Oncotarget. 2016; 7:52673-52684. https://doi.org/10.18632/oncotarget.10170

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Yu-ning Chen1,2, Meng-yun Cai1,2, Shun Xu1,2,3, Mei Meng1,2, Xingcong Ren4, Jay W. Yang4, Yu-qi Dong1,2, Xinguang Liu1,2,3, Jin-Ming Yang4 and Xing-dong Xiong1,2,3,4

1 Institute of Aging Research, Guangdong Medical University, Dongguan, Guangdong, P.R.China

2 Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Dongguan, P.R.China

3 Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Zhanjiang, P.R.China

4 Department of Pharmacology and The Penn State Hershey Cancer Institute, The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center, Hershey, PA, USA

Correspondence to:

Xing-dong Xiong, email:

Jin-Ming Yang, email:

Keywords: lncRNA; AK156230; cellular senescence; mouse embryonic fibroblasts; autophagy; Gerotarget

Received: October 09, 2015 Accepted: June 06, 2016 Published: June 19, 2016


Long noncoding RNAs (lncRNAs) have gained extensive attentions in recent years because of their potential importance in a variety of biological and pathological processes. In this study, we sought to explore the role of lncRNAs in cellular senescence. Here, we report that the lncRNA AK156230 was downregulated during replicative senescence in mouse embryonic fibroblasts (MEFs), and knockdown of AK156230 promotes a robust senescence phenotype, including increase in the numbers of the senescence-associated β-galactosidase-positive cells, decrease of cell proliferation, accumulation of cells in the G2/M phase and reduction of autophagic activity. The cells with knockdown AK156230 expression also exhibited increased levels of p21, p53 and phosphorylated p53, and a decreased activity of CDK1. Moreover, rapamycin-induced autophagy offered cytoprotective effect and rescued cellular senescence in AK156230 knockdown cells. Gene expression profile showed that the dysregulation of autophagy and cell cycle genes contributed to the induction of cellular senescence after AK1561230 silencing. Taken together, these results suggest that downregulation of AK156230 is involved in the induction of cellular senescence through its roles in autophagy and cell cycle progression. Our study identifies AK156230 as a critical lncRNA that has a role in regulating cellular senescence in MEFs.

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