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. 2015 Mar 30;16(4):7112–7132. doi: 10.3390/ijms16047112

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

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miR-16 regulates cyclin E1 in breast cancer cells. (A) Northern analysis of miR-16 level in a nontumorigenic breast epithelial cell line (MCF10A) and three different breast cancer cell lines (MCF7, SKBR3, and Hs578T). Blot was reprobed for U6 snRNA. Bottom numbers are density relative to MCF10A cells after normalization to U6 snRNA; (B–D) The indicated breast cancer cell lines were transfected with control miRNA (ctrl), miR-16 precursor (pre) or antagomir (anti). The level of cyclin E1, HuR and loading control actin were assessed by western blot analysis (top). Numbers 1–3 represent three separate experiments. Cyclin E1 and HuR western blot signals were quantified by densitometry (bottom). Values are the means ± SD from three independent experiments. * p < 0.05 versus ctrl; ** p < 0.01 versus ctrl.

miR-16 regulates cyclin E1 in breast cancer cells. (A) Northern analysis of miR-16 level in a nontumorigenic breast epithelial cell line (MCF10A) and three different breast cancer cell lines (MCF7, SKBR3, and Hs578T). Blot was reprobed for U6 snRNA. Bottom numbers are density relative to MCF10A cells after normalization to U6 snRNA; (B–D) The indicated breast cancer cell lines were transfected with control miRNA (ctrl), miR-16 precursor (pre) or antagomir (anti). The level of cyclin E1, HuR and loading control actin were assessed by western blot analysis (top). Numbers 1–3 represent three separate experiments. Cyclin E1 and HuR western blot signals were quantified by densitometry (bottom). Values are the means ± SD from three independent experiments. * p < 0.05 versus ctrl; ** p < 0.01 versus ctrl.