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. 2018 Jul 3;53(3):1013–1026. doi: 10.3892/ijo.2018.4467

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Copyright: © Dong et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Knockdown of long non-coding RNA-SNHG14 in exosomes partially reverses trastuzumab resistance. (A) The silencing efficacy was evaluated via transfection of three siRNAs targeting SNHG14. (B) Knockdown of exosomal SNHG14 increased the proportion of cell death induced by treatment with trastuzumab in the two trastuzumab-resistant cell lines. (C) Western blotting was used to evaluate the effect of SNHG14-knockdown on c-PARP and caspase-3. (D) Flow cytometry assay of cellular apoptosis caused by knockdown of SNHG14. (E) si-SNHG14 #1 abrogated the improved invasive ability due to trastuzumab in the two cell lines (×20 magnification). ^*P<0.05; ^**P<0.01; ^***P<0.001 vs. respective si-NC group. si, small interfering; SNGH14, small nucleolar RNA host gene 14, c, cleaved; NC, negative control; PARP, poly(ADP-ribose) polymerase.