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LncRNA TUG1 promotes tumor growth and metastasis of esophageal squamous cell carcinoma by regulating XBP1 via competitively binding to miR-498  ( SCI-EXPANDED收录)   被引量:17

文献类型:期刊文献

英文题名:LncRNA TUG1 promotes tumor growth and metastasis of esophageal squamous cell carcinoma by regulating XBP1 via competitively binding to miR-498

作者:Jin, G.[1];Yang, Y.[2];Tuo, G.[2];Wang, W.[1];Zhu, Z.[1]

第一作者:Jin, G.

通信作者:Zhu, Z[1]

机构:[1]Gansu Prov Hosp, Dept Thorac Surg 2, Lanzhou, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Dept Clin Med, Lanzhou, Peoples R China

第一机构:Gansu Prov Hosp, Dept Thorac Surg 2, Lanzhou, Peoples R China

通信机构:[1]corresponding author), Gansu Prov Hosp, Dept Thorac Surg 2, Lanzhou, Peoples R China.

年份:2020

卷号:67

期号:4

起止页码:751

外文期刊名:NEOPLASMA

收录:;Scopus(收录号:2-s2.0-85088628345);WOS:【SCI-EXPANDED(收录号:WOS:000557901000005)】;

语种:英文

外文关键词:esophageal squamous cell carcinoma; TUG1; miR-498; XBP1

摘要:Esophageal squamous cell carcinoma (ESCC) is a major subtype of esophageal cancer with high mortality. Previous reports suggested that lncRNA taurine upregulated gene 1 (TUG1) functioned as an oncogene in numerous cancers. The purpose of this study was to explore the potential mechanism of TUG1 carcinogenesis in ESCC. The expression of TUG1 and miR-498 was measured by a quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry. Cell migration and invasion were identified through the transwell assay. The interaction between miR-498 and TUG1 or X-box binding protein 1 (XBP1) was predicted by bioinformatics software starBase and verified by luciferase reporter assay. The expression of XBP1 was quantified by qRT-PCR and western blot analysis. Xenograft tumor mouse model was established to determine the function of TUG1 in vivo. TUG1 was upregulated in ESCC tissues and cells, and its high expression was associated with tumor lymph node metastasis and low cumulative survival. TUG1 knockdown inhibited proliferation, migration, and invasion but promoted apoptosis in ESCC cells. It was confirmed that miR-498 was a target of TUG1, and XBP1 was a target of miR-498. The expression of miR-498 was reduced in ESCC tissues while XBP1 expression was notably enhanced. Mechanism analysis manifested that TUG1 regulated proliferation, apoptosis, migration, and invasion by upregulating XBP1 via targeting miR-498 in vitro. Furthermore, knockdown of TUG1 attenuated tumor growth in vivo. TUG1 accelerated tumorigenesis and metastasis by inducing XBP1 expression through directly targeting miR-498 in ESCC.

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