The long non-coding RNA NEAT1 enhances epithelial-to-mesenchymal transition and chemoresistance via the miR-34a/c-Met axis in renal cell carcinoma

被引:61
作者
Liu, Fei [1 ]
Chen, Na [2 ]
Gong, Yanchun [3 ]
Xiao, Ruihai [1 ]
Wang, Weichao [1 ]
Pan, Zhengyue [1 ]
机构
[1] Nanchang Univ, Affiliated Hosp 2, Dept Urol, Nanchang 330006, Jiangxi, Peoples R China
[2] Nanchang Univ, Affiliated Hosp 4, Dept Breast Surg, Nanchang 330003, Jiangxi, Peoples R China
[3] Jiangxi Sci & Technol Normal Univ, Sch Life Sci, Nanchang 330013, Jiangxi, Peoples R China
关键词
renal cell carcinoma; NEAT1; miR-34a; c-Met; chemotherapy; CANCER STATISTICS; INVASION; METASTASIS; RESISTANCE; MIGRATION; PROLIFERATION; PROGRESSION; EXPRESSION; SORAFENIB;
D O I
10.18632/oncotarget.17757
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long non-coding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in various cancers. Although the lncRNA nuclear enriched abundant transcript 1 (NEAT1) has been associated with tumorigenesis, its functions in renal cell carcinoma (RCC) have not been elucidated. We determined that NEAT1 is up-regulated in RCC tissue compared to corresponding non-tumor tissue. High NEAT1 expression was associated with tumor progression and poor survival in RCC patients. NEAT1 knockdown suppressed RCC cell proliferation by inhibiting cell cycle progression, and inhibited RCC cell migration and invasion by reversing the epithelial-to-mesenchymal transition phenotype. Down-regulation of NEAT1 increased the sensitivity of RCC cells to sorafenib in vitro. Mechanistic analysis revealed that NEAT1 acts as a competitive sponge for miR-34a, which prevents inhibition of c-Met. Thus, NEAT1 promotes RCC progression through the miR-34a/c-Met axis.
引用
收藏
页码:62927 / 62938
页数:12
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