Research Papers:

MicroRNA-410 acts as oncogene in NSCLC through downregulating SLC34A2 via activating Wnt/β-catenin pathway

Xuechao Zhang, Xixian Ke, Qiang Pu, Yue Yuan, Weihan Yang, Xinmei Luo, Qianqian Jiang, Xueting Hu, Yi Gong, Kui Tang, Xiaolan Su, Lunxu Liu, Wen Zhu _ and Yuquan Wei

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Oncotarget. 2016; 7:14569-14585. https://doi.org/10.18632/oncotarget.7538

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Xuechao Zhang1,*, Xixian Ke1,*, Qiang Pu2, Yue Yuan1, Weihan Yang1, Xinmei Luo1, Qianqian Jiang1, Xueting Hu1, Yi Gong1, Kui Tang1, Xiaolan Su1, Lunxu Liu2, Wen Zhu1 and Yuquan Wei1

1 State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan Province, People’s Republic of China

2 Department of Thoracic Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, People’s Republic of China

* These authors have contributed equally to this work

Correspondence to:

Wen Zhu, email:

Lunxu Liu, email:

Keywords: miR-410, SLC34A2, NSCLC, tumorigenesis and development

Received: July 30, 2015 Accepted: December 31, 2015 Published: February 20, 2016


SLC34A2 had been reported to be down-regulated in human NSCLC cells and patient tissues, and played a significant role in lung cancer. However, the mechanism of its unusual expressionin NSCLC has not been fully elucidated. In present study, we identified SLC34A2 was a direct target of miR-410 and could be inhibited by miR-410 transcriptionally and post-transcriptionally. MiR-410 promoted the growth, invasion and migration of NSCLC cells in vitro. An orthotopic xenograft nude mouse model further affirmed that miR-410 promoted NSCLC cell growth and metastasis in vivo. Moreover, restoring SLC34A2 expression effectively reversed the miR-410-mediated promotion of cell growth, invasion and migration in NSCLC cells. In addition, miR-410high /SLC34A2low expression signature frequently existed in NSCLC cells and tumor tissues. MiR-410 significantly increased the expression of DVL2 and β-catenin protein while decreased that of Gsk3β protein of Wnt/β-catenin signaling pathway, while SLC34A2 partly blocked the effects of miR-410 on those protein expressions. Hence, our data for the first time delineated that unusual expression of SLC34A2 was modulated by miR-410, and miR-410 might positivelycontribute to the tumorigenesis and development of NSCLC by down-regulating SLC34A2 and activating Wnt/β-catenin signaling pathway. MiR-410 might be a new potential therapeutic target for NSCLC.

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