The long non-coding RNA NEAT1 enhances epithelial-to-mesenchymal transition and chemoresistance via the miR-34a/c-Met axis in renal cell carcinoma
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Fei Liu1,*, Na Chen2,*, Yanchun Gong3, Ruihai Xiao1, Weichao Wang1 and Zhengyue Pan1
1Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China
2Department of Breast Surgery, The Fourth Affiliated Hospital of Nanchang University, Nanchang 330003, China
3School of Life Science, Jiangxi Science and Technology Normal University, Nanchang 330013, China
*These authors have contributed equally to this work
Fei Liu, email: [email protected]
Keywords: renal cell carcinoma, NEAT1, miR-34a, c-Met, chemotherapy
Received: December 08, 2016 Accepted: March 15, 2017 Published: May 10, 2017
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.
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