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. 2020 Sep 3;10:14584. doi: 10.1038/s41598-020-71128-1

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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A schematic diagram illustrating miR-107 and GRN function in the balance between radiosensitivity and radioresistance in PC-3 cells. Left: MiR-107 is repressed and GRN induced in PC-3 cells following exposure to IR. p21 and CHK2, both cell cycle regulators, is activated or phosphorylated in response to DNA damage induced by IR, resulting in G1/S and G2/M arrest, which allows for repair of DNA damage and maintenance of genomic integrity. Right: Elevated miR-107 represses GRN expression by directly targeting GRN mRNA. Upon miR-107 overexpression and GRN knockdown, flow cytometry showed more prominent G1/S arrest and/or G2 check point abrogation (G2/M transit), and annexin V binding assays revealed delayed apoptosis after IR. Consequently, miR-107 sensitizes cancer cells to IR by down-regulating the p21 pathway or directly repressing CHK2 phosphorylation to modulate cell cycle checkpoint function.