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. 2019 Feb 22;6(8):1801927. doi: 10.1002/advs.201801927

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© 2019 The Authors. Published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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ATG7 was an MIR190A downstream effector responsible for BC invasion. A,B) The invasion abilities of the indicated cells were evaluated. Student's t‐test was utilized to determine the p‐value; the asterisk (*) indicates a significant increase in comparison to UMUC3(pLKO.1) transfectants (*p < 0.05) (B), while the double asterisk (**) indicates a significant decrease in comparison to UMUC3(LacZ) transfectants (**p < 0.05). C) ATG7 overexpressed plasmid was stably transfected into UMUC3(Anti‐MIR190A) cells. The overexpression efficiency of ATG7 protein was assessed by Western Blotting. β‐Actin was used as an internal protein loading control. D) The invasion abilities of UMUC3(Anti‐MIR190A) and UMUC3(Anti‐MIR190A/ATG7) cells were evaluated. Student's t‐test was utilized to determine the p‐value; the double asterisk (**) indicates a significant decrease in comparison to scramble vector transfectants (**p < 0.05), while the asterisk (*) indicates a significant increase in comparison to Anti‐MIR190A transfectants (*p < 0.05) (E).