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. 2020 Jul 30;11(7):602. doi: 10.1038/s41419-020-02812-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — a Interference with either DNA-PKcs or miR-1193 alone did not reduce the viability of cancer cells, while cell death was achieved by combined abolition of DNA-PKcs and miR-1193. b Function loss of DNA-PKcs resulted in dysregulation of the NHEJ-mediated DSB repair pathway (left panel). Inhibition of miR-1193 led to blockade of the FEN1-mediated HR/MMEJ repair pathway (middle panel). Combined abolition of DNA-PKcs and miR-1193 promoted DSB repair deficiency and induced apoptosis regulated by the ATR/CHK1/p53 axis (right panel).