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MiR-107 suppresses cell proliferation and tube formation of Ewing sarcoma cells partly by targeting HIF-1β

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Abstract

MicroRNAs serve a crucial role in the regulation of malignant biological behavior of Ewing’s sarcoma (ES). Abnormal expression of miR-107 has been reported in a cohort of cancers, while its exact function in ES remains unclear. Hence, we explored the expression of miR-107 in ES cells and detected its effects on the malignant phenotype of ES cells. Firstly, we perceived the under-expression of miR-107 in human ES cells contrast with the human mesenchymal stem cells. Over-expression of miR-107 restrained cell proliferation and tube formation, arrested cell cycle progression, and facilitated cell apoptosis in SK-ES-1 and RD-ES cell lines. Furthermore, hypoxia inducible factor-1β (HIF-1β) was assumed as a target gene of miR-107. We confirmed the target role of HIF-1β in ES cells. Finally, restoring the expression of HIF-1β could partly abolish miR-107-mediated tumor suppression in ES cells. In conclusion, our results advised that miR-107 suppressed the malignant biological ability of ES cells through targeting HIF-1β.

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Acknowledgements

This project is Funded by the National Nature Science Foundation of China (Grant No. 81502329); Program of Science and Technology of ChongQing Commission (Grant No. KJ1600228); Programs of Yongchuan Hospital of ChongQing Medical University (Grant Nos. YJZQN 201514; YCZQN201511).

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Correspondence to Yunyun Li or Zhongzu Zhang.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the Ethics Committee of Chongqing Medical University and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

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Informed consent was obtained from all individual participants included in the study.

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Chen, J., Zhou, X., Xiao, Q. et al. MiR-107 suppresses cell proliferation and tube formation of Ewing sarcoma cells partly by targeting HIF-1β. Human Cell 31, 42–49 (2018). https://doi.org/10.1007/s13577-017-0183-9

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  • DOI: https://doi.org/10.1007/s13577-017-0183-9

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