Research Papers:

Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer

Wen-ming Chen, Ming-de Huang, Dao-ping Sun, Rong Kong, Tong-peng Xu, Rui Xia, Er-bao Zhang and Yong-qian Shu _

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Oncotarget. 2016; 7:9773-9787. https://doi.org/10.18632/oncotarget.6949

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Wen-ming Chen1,*, Ming-de Huang2,*, Dao-ping Sun1,*, Rong Kong3, Tong-peng Xu4, Rui Xia5, Er-bao Zhang5, Yong-qian Shu4

1Department of Oncology, Jining NO.1 People’s Hospital, Jining City, Shandong Province 272011, China

2Department of Medical Oncology, Huai’an First People’s Hospital, Nanjing Medical University, Jiangsu Province 223300, China

3Central Laboratory, Subei People's Hospital of Jiangsu province, Yangzhou, Jiangsu Province 225001, China

4Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, Jiangsu Province 210029, China

5Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China

*These authors have contributed equally to this work

Correspondence to:

Yong-qian Shu, e-mail: [email protected]

Keywords: long non-coding RNA, LINC00152, gastric cancer, cell proliferation, p15/p21

Received: May 01, 2015     Accepted: December 28, 2015     Published: January 19, 2016


Long noncoding RNAs (lncRNAs) play important regulatory roles in several human cancers. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LINC00152 expression was positively correlated with tumor invasion depth, lymph node metastasis, higher TNM stage, and poor survival. Gene set enrichment analysis revealed that cell proliferation and cell cycle progression were increased in patients with high LINC00152 expression. In both GC cell lines and xenograft systems, LINC00152 overexpression facilitated GC cell proliferation by accelerating the cell cycle, whereas LINC00152 knockdown had the opposite effect. Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21. These findings suggest that LINC00152 may play contribute to the progression of GC and may be an effective therapeutic target.

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