Research Papers:

Upregulation of long noncoding RNA HOTTIP promotes metastasis of esophageal squamous cell carcinoma via induction of EMT

Xuemei Chen, Hongyu Han, Yuqi Li, Qiongxia Zhang, Kailan Mo and Size Chen _

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Oncotarget. 2016; 7:84480-84485. https://doi.org/10.18632/oncotarget.12995

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Xuemei Chen1, Hongyu Han2, Yuqi Li3, Qiongxia Zhang3, Kailan Mo3, Size Chen3

1School of Public Health, Southern Medical University, Guangzhou, 510515, China

2Cancer Center, Sun Yat-Sen University, Guangzhou, 510080, China

3Department of Oncology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China

Correspondence to:

Size Chen, email: [email protected]

Keywords: HOTTIP, long noncoding RNA, ESCC, proliferation, EMT

Received: July 06, 2016     Accepted: October 13, 2016     Published: October 31, 2016


Esophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide, especially in Eastern Asia. The prognosis of ESCC remains poor; thus, it is still necessary to further dissect the underlying mechanisms and explore therapeutic targets of ESCC. Recent studies show that lncRNAs involve in the initiation and progression of various cancers including ESCC. HOTTIP has been recently revealed as oncogenic regulator in different cancers, however, whether HOTTIP is involved in ESCC remains poorly understood. To investigate the role of HOTTIP in ESCC, we evaluated the HOTTIP expression levels in a series of ESCC tissues and a panel of ESCC cell line using qRT-PCR. Moreover, we investigated the effect of HOTTIP on cell proliferation, migration and invasion of ESCC cells. Here, we reported that HOTTIP was upregulated in ESCC. Further experiments revealed that HOTTIP knockdown significantly inhibited ESCC cells proliferation by causing G1 arrest. Furthermore, inhibitory effects of HOTTIP on cell migration and invasion were partly associated with EMT process. In conclusion, these data suggest that HOTTIP could be an oncogene for ESCC, and may be served as a candidate target for new therapies in human ESCC.

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