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miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS

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Abstract

MicroRNAs have been implicated in regulating diverse cellular pathways. Emerging evidence indicates that miR-143 plays causal roles in cancer tumorigenesis as a tumor suppress gene; however, its role in prostate cancer tumorigenesis remains largely unknown. The aims of this study were to verify the effect of miR-143 on proliferation and migration abilities of prostate cancer cells. The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting, respectively. Effects of miR-143 in cell proliferation, migration and chemosensitivity were evaluated by MTT assay, FACS cell cycle analysis, colony formation assay, and transwell migratory assay. Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples (Pearson’s correlation scatter plots: R = −0.707, P < 0.05). Moreover, over-expression of miR-143 in prostate cancer cells suppressed their proliferation and migration and increased their sensitivity to docetaxel by targeting EGFR/RAS/MAPK pathway. These findings suggest that miR-143 plays an important role in prostate cancer proliferation, migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway, which provides a potential development of a new approach for the treatment of prostate cancer.

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Acknowledgments

This study was supported by National Natural Science Foundation of China (No. 30872575), Health Project of Jiangsu Province (XK17 20090), and National Eleventh-Five Science and Technology Support Program of China (No. 2006BAI03B12).

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There are no financial or other interests with regard to the paper that represent a conflict of interest.

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Correspondence to Zengjun Wang.

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Autuhors Bin Xu, Xiaobing Niu, and Xiangxiang Zhang contributed equally to this work.

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Xu, B., Niu, X., Zhang, X. et al. miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS. Mol Cell Biochem 350, 207–213 (2011). https://doi.org/10.1007/s11010-010-0700-6

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  • DOI: https://doi.org/10.1007/s11010-010-0700-6

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