Research Papers:

Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer

Xuefei Shi, Chenhui Ma, Qingqing Zhu, Dongmei Yuan, Ming Sun, Xiaoling Gu, Guannan Wu, Tangfeng Lv _ and Yong Song

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Oncotarget. 2016; 7:25558-25575. https://doi.org/10.18632/oncotarget.8338

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Xuefei Shi1,3,*, Chenhui Ma1,*, Qingqing Zhu1, Dongmei Yuan1, Ming Sun2, Xiaoling Gu1, Guannan Wu1, Tangfeng Lv1, Yong Song1

1Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China

2Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China

3Department of Respiratory Medicine, Huzhou Central Hospital, Huzhou, China

*These authors have contributed equally to this work

Correspondence to:

Tangfeng Lv, e-mail: [email protected]

Yong Song, e-mail: [email protected]

Keywords: linc00673, proliferation, LSD1, NCALD, NSCLC

Received: December 14, 2015     Accepted: March 07, 2016     Published: March 24, 2016


Despite improvements in diagnostics and treatment of non-small cell lung cancer (NSCLC), it remains the leading causes of cancer-related mortality worldwide. In more recent years, mutiple lines of evidence have highlighted long noncoding RNAs (lncRNAs) serve as novel class of regulators of cancer biological processes, including proliferation, apoptosis and metastasis. LncRNAs serve as a novel class of regulators of cancer biological processes in cancer, but little is known of their expression and potential functions in NSCLC. We identified an oncogene, linc00673, whose expression level was upregulated by bioinformatics analyses and qRT-PCR analyses in NSCLC. The effects of linc00673 on tumor progression were investigated in vitro and in vivo. Linc00673 knockdown significantly inhibited cell proliferation and colony-forming ability, and suppressed S-phase entry in vitro and shRNA linc00673 mediated knockdown significantly inhibit tumor growth in vivo, meanwhile, linc00673 overexpression increased tumor cell growth. Analysis of RNAseq data revealed linc00673 could modulate the transcription of a large amount of genes including oncogene and tumor suppressor gene, so we investigated the role and regulatory mechanism of linc00673 in NSCLC proliferation. Further mechanistic analyses indicated that the oncogenic activity of linc00673 is partially attributable to its repression of NCALD through association with the epigenetic repressor LSD1. Taken together, these findings suggested that linc00673 could play crucial role in NSCLC progression and might be a potential therapeutic target for patients with NSCLC.

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