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miR-411 contributes the cell proliferation of lung cancer by targeting FOXO1

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Tumor Biology

Abstract

Lung cancer is the leading cause of cancer deaths worldwide; the study of microRNAs gives new hope for lung cancer treatment. miR-411 has been demonstrated to be an independent prognostic factor for lung adenocarcinoma, but the role and regulatory mechanism are largely unknown. In the present study, we found miR-411 was overexpressed in the lung cancer cells; overexpression of miR-411 promoted anchorage-dependent and anchorage-independent growths of lung cancer, while miR-411 knockdown reduced this effect. Further study showed forkhead box O1 (FOXO1) was a target of miR-411. Overexpression of miR-411 suppressed the expression of FOXO1; the effect of suppression was abrogated when the mutation occurred in the 3′UTR of FOXO1. Knockdown of FOXO1 in cells which miR-411 was inhibited recapitulated the phenotype of miR-411 overexpression. Taken together, our study revealed miR-411 promoted cell proliferation of lung cancer by targeting tumor suppressor gene FOXO1 and miR-411 might be a potential target for lung cancer therapy.

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Acknowledgments

This work was supported by grants from the Science and technology project of Guangdong Province grant (No.2014A020212640, LM Qin).

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Correspondence to Zhiju Zhao.

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Supplemental Figure 1

miR-411 regulates cell proliferation of BEAS-2B. (A). MTT assay determined the effect on the proliferation after miR-411 was downregulated in BEAS-2B. (B). Colony formation assay determined the effect on the proliferation after miR-411 was downregulated in BEAS-2B. (C). Real-time quantitative PCR analysis determined the expression of cell cycle regulator, p21, p27 and Cyclin D1 transfected miR-411 inhibitor. *p < 0.05, Error bars represent mean ± STDEV . (GIF 4.67 mb)

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Zhao, Z., Qin, L. & Li, S. miR-411 contributes the cell proliferation of lung cancer by targeting FOXO1. Tumor Biol. 37, 5551–5560 (2016). https://doi.org/10.1007/s13277-015-4425-8

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