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. 2021 Apr 29;40(20):3510–3532. doi: 10.1038/s41388-021-01698-5

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© The Author(s) 2021

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. 2 — A MRE11 knockdown decreased, while its overexpression increased, wound closure in oral cancer cells. B MRE11 knockdown decreased, while its overexpression increased, transwell migration in oral cancer cells. C MRE11 knockdown decreased, while its overexpression increased, transwell invasion in oral cancer cells. D MRE11 knockdown decreased, while its overexpression increased, epithelial-to-mesenchymal transition in oral cancer cells. E Mirin, a MRE11 nuclease inhibitor, increased the expression of γH2AX, an indicator of DSB, in oral cancer cells upon ionizing radiation exposure. F Mirin treatment did not inhibit the proliferation-promoting activity of MRE11 in oral cancer cells. G Mirin treatment did not inhibit the migration-promoting activity of MRE11 in oral cancer cells. H Nuclease-deficient MRE11 with H129N mutation showed proliferation-promoting activity. I Nuclease-deficient MRE11 with H129N mutation showed migration-promoting activity.

Fig. 2 — A MRE11 knockdown decreased, while its overexpression increased, wound closure in oral cancer cells. B MRE11 knockdown decreased, while its overexpression increased, transwell migration in oral cancer cells. C MRE11 knockdown decreased, while its overexpression increased, transwell invasion in oral cancer cells. D MRE11 knockdown decreased, while its overexpression increased, epithelial-to-mesenchymal transition in oral cancer cells. E Mirin, a MRE11 nuclease inhibitor, increased the expression of γH2AX, an indicator of DSB, in oral cancer cells upon ionizing radiation exposure. F Mirin treatment did not inhibit the proliferation-promoting activity of MRE11 in oral cancer cells. G Mirin treatment did not inhibit the migration-promoting activity of MRE11 in oral cancer cells. H Nuclease-deficient MRE11 with H129N mutation showed proliferation-promoting activity. I Nuclease-deficient MRE11 with H129N mutation showed migration-promoting activity.