lncRNA ROR promotes the progression of renal cell carcinoma through the miR‑206/VEGF axis
- Jianguo Shi
- Datian Zhang
- Zhenhai Zhong
- Wen Zhang
Published online on: September 2, 2019
Copyright: © Shi et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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Renal cell carcinoma (RCC) is the most common kidney malignancy, responsible for ~80% of all cases in adults. The pathogenesis of RCC is complex, involving alterations at both the genetic and epigenetic levels. Numerous signaling pathways, such as PI3K/Akt/mTOR and Wnt‑β‑catenin have been demonstrated to be associated with the tumorigenesis and development of RCC. Long non‑coding RNAs (lncRNAs) are functional RNA molecules involved in the initiation and progression of cancer, and investigating the effects of lncRNA could facilitate the development of novel treatments. The lncRNA regulator of reprogramming (ROR) is aberrantly expressed in a variety of tumors. However, its underlying mechanisms remain largely unknown. In the present study, ROR was found to be upregulated and microRNA (miR)‑206 was found to be downregulated in RCC tissues and cells. Furthermore, the knockdown of ROR inhibited the proliferation, migration and invasion of RCC cells. It was found that ROR binds to miR‑206, and that ROR‑induced cell proliferation and metastasis were reversed by the overexpression of miR‑206. In addition, the levels of miR‑206 and ROR were negatively correlated in RCC tissues. Furthermore, the overexpression of miR‑206 notably suppressed the proliferation, migration and invasion of RCC cells, and these effects were enhanced by the knockdown of vascular endothelial growth factor (VEGF); cell growth and metastasis induced by miR‑206 inhibitors could be reversed by the knockdown of VEGF. In addition, the expression levels of miR‑206 and VEGF were inversely correlated in RCC samples. In summary, the results of the present study revealed that ROR was upregulated in RCC tissues, which promoted tumor progression by regulating the miR‑206/VEGF axis. The present findings provided a novel insight into the potential functions of ROR in RCC, and the ROR/miR‑206/VEGF pathway may be a promising therapeutic target for the treatment of patients with RCC.