Research Papers:

A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer

Yifan Lian, Changsheng Yan, Jie Ding, Rui Xia, Zhonghua Ma, Bingqing Hui, Hao Ji, Jing Zhou and Keming Wang _

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Oncotarget. 2017; 8:59435-59445. https://doi.org/10.18632/oncotarget.19738

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Yifan Lian1,2,*, Changsheng Yan3,*, Jie Ding4,*, Rui Xia5, Zhonghua Ma1,4, Bingqing Hui1,4, Hao Ji1,4, Jing Zhou1,4 and Keming Wang1,4

1The Second Clinical Medical College of Nanjing Medical University, Nanjing 210000, Jiangsu, People’s Republic of China

2Department of Gastroenterology, Zhongshan Hospital Affiliated to Xiamen University, Xiamen 361004, Fujian, People’s Republic of China

3Department of Obstetrics and Gynecology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, Jiangsu, People’s Republic of China

4Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing 210000, Jiangsu, People’s Republic of China

5Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210000 Jiangsu, People’s Republic of China

*These authors have contributed equally to this work

Correspondence to:

Keming Wang, email: [email protected]

Keywords: colorectal cancer, proliferation, LL22NC03-N64E9.1, KLF2, lncRNA

Received: October 25, 2016     Accepted: June 12, 2017     Published: July 31, 2017


Long noncoding RNAs (lncRNA) have been implicated in variety human cancer but their mechanisms of function are mainly undocumented. In the present study, we investigated lncRNAs alteration that contributed to colorectal cancer (CRC) by utilizing TCGA RNA sequencing data and other publicly available lncRNAs expression profiling data. Here, We screened out the CRC–associated lncRNA LL22NC03-N64E9.1, a key regulator of CRC development and progression. We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2. Taken together, our results suggested that LL22NC03-N64E9.1 confered an oncogenic function in human CRC and may serve as a candidate prognostic biomarker and target for new therapies in this deadly disease.

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