Research Papers:

Tumor-suppressive miR-218-5p inhibits cancer cell proliferation and migration via EGFR in non-small cell lung cancer

Kegan Zhu, Hanying Ding, Wengong Wang, Zhicong Liao, Zheng Fu, Yeting Hong, Yong Zhou, Chen-Yu Zhang and Xi Chen _

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Oncotarget. 2016; 7:28075-28085. https://doi.org/10.18632/oncotarget.8576

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Kegan Zhu1,*, Hanying Ding1,*, Wengong Wang2,*, Zhicong Liao1, Zheng Fu1, Yeting Hong1, Yong Zhou2, Chen-Yu Zhang1, Xi Chen1

1State Key Laboratory of Pharmaceutical Biotechnology, Collaborative Innovation Center of Chemistry for Life Sciences, NJU Advanced Institute for Life Sciences (NAILS), Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210046, China

2Department of Thoracic and Cardiovascular Surgery, Department of General Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China

*These authors have contributed equally to this work

Correspondence to:

Xi Chen, email: [email protected]

Chen-Yu Zhang, email: [email protected]

Yong Zhou, email: [email protected]

Keywords: NSCLC, miR-218-5p, EGFR, proliferation, migration

Received: February 02, 2016     Accepted: March 28, 2016     Published: April 4, 2016


Lung cancer remains the leading cause of cancer-related death worldwide, and non-small cell lung cancer (NSCLC) accounts for approximately 80% of lung cancer cases. Recently, microRNAs (miRNAs) have been consistently demonstrated to be involved in NSCLC and to act as either tumor oncogenes or tumor suppressors. In this study, we identified a specific binding site for miR-218-5p in the 3’-untranslated region of the epidermal growth factor receptor (EGFR). We further experimentally validated miR-218-5p as a direct regulator of EGFR. We also identified an inverse correlation between miR-218-5p and EGFR protein levels in NSCLC tissue samples. Moreover, we demonstrated that miR-218-5p plays a critical role in suppressing the proliferation and migration of lung cancer cells probably by binding to EGFR. Finally, we examined the function of miR-218-5p in vivo and revealed that miR-218-5p exerts an anti-tumor effect by negatively regulating EGFR in a xenograft mouse model. Taken together, the results of this study highlight an important role for miR-218-5p in the regulation of EGFR in NSCLC and may open new avenues for future lung cancer therapies.

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