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长链非编码RNA SPRY4-IT1促进胆囊癌进展。

Long non-coding RNA SPRY4-IT1 promotes gallbladder carcinoma progression.

作者信息

Yang Liang, Cheng Xi, Ge Naijian, Guo Weixing, Feng Feiling, Wan Fuying

机构信息

Radiation Center, East Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 201805, China.

Mini-Invasive Intervention Center, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China.

出版信息

Oncotarget. 2017 Jan 10;8(2):3104-3110. doi: 10.18632/oncotarget.13621.

Abstract

Gallbladder carcinoma (GBC) is the most common malignancy of the bile duct and patients with GBC have extremely poor prognoses. Long non-coding RNAs (lncRNAs) are found to be dysregulated in a variety of cancers, including GBC. SPRY4-IT1 has been recently revealed as oncogenic regulator in many cancers. However, whether SPRY4-IT1 is involved in GBC progression remains largely unknown. To investigate the role of SPRY4-IT1 in GBC, we evaluated the expression SPRY4-IT1 in GBC tissues and cell lines, and investigated the effect of SPRY4-IT1 knockdown on cell proliferation, migration and invasion of GBC in vitro. Our result showed that SPRY4-IT1 was upregulated in GBC tissues. Further experiments revealed that SPRY4-IT1 knockdown significantly inhibited GBC cell proliferation. Furthermore, inhibitory effects of SPRY4-IT1 on cell migration and invasion were partly associated with EMT process. In conclusion, these data suggest that SPRY4-IT1 could be an oncogene for GBC, and may be served as a candidate target for new therapies in human GBC.

摘要

胆囊癌(GBC)是胆管最常见的恶性肿瘤,GBC患者的预后极差。长链非编码RNA(lncRNAs)在包括GBC在内的多种癌症中表达失调。SPRY4-IT1最近被揭示为许多癌症中的致癌调节因子。然而,SPRY4-IT1是否参与GBC进展在很大程度上仍不清楚。为了研究SPRY4-IT1在GBC中的作用,我们评估了SPRY4-IT1在GBC组织和细胞系中的表达,并研究了敲低SPRY4-IT1对GBC细胞体外增殖、迁移和侵袭的影响。我们的结果表明,SPRY4-IT1在GBC组织中上调。进一步的实验表明,敲低SPRY4-IT1可显著抑制GBC细胞增殖。此外,SPRY4-IT1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,SPRY4-IT1可能是GBC的一个癌基因,并可能作为人类GBC新疗法的候选靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6c/5356867/f1a9d954a57e/oncotarget-08-3104-g001.jpg

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