A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer
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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
Keming Wang, email: firstname.lastname@example.org
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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