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. 2019 Nov 8;11(11):1762. doi: 10.3390/cancers11111762

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© 2019 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 (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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RRP1B mediates the down-regulation of DNMTs, the up-regulation of claudin-1, and increased cell viability caused by DOCK1 depletion. (A,B) Claudin-low breast cancer cells were treated with the shDOCK1 for three days. Cancer cells were collected for protein determination (A) or immunofluorescence staining (B). (B) RRP1B was stained with a specific anti-RRP1B antibody. Nuclei were counterstained with DAPI. Magnification, 400×. Scale bar = 25 μm. (C–H) Claudin-low breast cancer cells were treated with the shDOCK1, shRRP1B, or shJUN for three days followed by the protein determination (C,F–H), cell migration (D), or cell viability (E). The results are expressed as the mean ± SE from three independent experiments. * p < 0.05; ** p < 0.01, compared with the control (shLuc).