Research Papers:

miR-338-3p inhibits the invasion of renal cell carcinoma by downregulation of ALK5

Xiaoqian Zhang, Chunxia Wang, Hui Li, Xiaobin Niu, Xinwei Liu, Dongxu Pei, Xiaolan Guo, Xiaona Xu and Yongwei Li _

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Oncotarget. 2017; 8:64106-64113. https://doi.org/10.18632/oncotarget.19329

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Xiaoqian Zhang1, Chunxia Wang1, Hui Li1, Xiaobin Niu1, Xinwei Liu1, Dongxu Pei1, Xiaolan Guo1, Xiaona Xu1 and Yongwei Li1

1Department of Clinical Laboratory, Henan Province Hospital of TCM, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450002, Henan Province, China

Correspondence to:

Yongwei Li, email: [email protected]

Keywords: miR-338-3p, renal cell carcinoma (RCC), activin receptor-like kinase 5 (ALK5), invasion, metastasis

Abbreviations: renal cell carcinoma (RCC), quantitative reverse transcription-polymerase chain reaction (qRT-PCR), activin receptor-like kinase 5 (ALK5), microRNAs (miRNAs)

Received: May 09, 2017     Accepted: June 13, 2017     Published: July 18, 2017


Background: The current study aims to elucidate the role of miRNA-338-3p (miR-338-3p) in the invasion of renal cell carcinoma (RCC).

Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to detect the expression of miR-338-3p in human RCC cell lines with high metastatic potential (Caki-1) and low metastatic potential (786-O), respectively. The Caki-1 and 786-O cells were transfected with miR-338-3p mimic or inhibitor. Wound healing assay, Transwell assay and western blotting were performed to analyze the invasive ability and expression of activin receptor-like kinase 5 (ALK5) in the RCC cell lines. During the 36-month follow-up, we detected the expressions of miR-338-3p and ALK5 in 22 RCC cases with metastasis and 60 cases achieving a remission.

Results: miR-339-3p was significantly downregulated in the Caki-1 cells as compared with the 786-O cells. The transfection with miR-338-3p inhibitor caused an increased invasive ability of both two cell lines. However, the transfection with miR-338-3p mimic caused a reduction of the invasiveness. In RCC cells, the expression of ALK5 was negatively correlated to miR-338-3p. Upregulation of ALK5 partially counteracted the miR-338-3p-induced invasiveness of RCC cells. We subsequently found the negative correlations between miR-338-3p and metastasis/ALK5 expression could be also observed in human RCC tissues.

Conclusion: Taken together, these results indicate that miR-338-3p acts as a novel tumor suppressor to inhibit the invasion of RCC by regulating ALK5 expression.

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