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长链非编码RNA HOTTIP的上调通过诱导上皮-间质转化促进食管鳞状细胞癌的转移。

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

作者信息

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

机构信息

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

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

出版信息

Oncotarget. 2016 Dec 20;7(51):84480-84485. doi: 10.18632/oncotarget.12995.

Abstract

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.

摘要

食管鳞状细胞癌(ESCC)是全球范围内常见且致命的癌症之一,尤其是在东亚地区。ESCC的预后仍然很差;因此,进一步剖析其潜在机制并探索ESCC的治疗靶点仍然很有必要。最近的研究表明,长链非编码RNA(lncRNAs)参与包括ESCC在内的各种癌症的发生和发展。HOTTIP最近被揭示为不同癌症中的致癌调节因子,然而,HOTTIP是否参与ESCC仍知之甚少。为了研究HOTTIP在ESCC中的作用,我们使用qRT-PCR评估了一系列ESCC组织和一组ESCC细胞系中的HOTTIP表达水平。此外,我们研究了HOTTIP对ESCC细胞增殖、迁移和侵袭的影响。在此,我们报道HOTTIP在ESCC中上调。进一步的实验表明,敲低HOTTIP可通过导致G1期阻滞显著抑制ESCC细胞增殖。此外,HOTTIP对细胞迁移和侵袭的抑制作用部分与上皮-间质转化(EMT)过程有关。总之,这些数据表明HOTTIP可能是ESCC的致癌基因,并可能作为人类ESCC新疗法的候选靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1c3/5356674/bdf8d4b01f73/oncotarget-07-84480-g001.jpg

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