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Supplementary Table 1, Figures 1 - 10 from MicroRNA-21 Modulates the Levels of Reactive Oxygen Species by Targeting SOD3 and TNFα

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posted on 2023-03-30, 21:13 authored by Xiangming Zhang, Wooi-Loon Ng, Ping Wang, LinLin Tian, Erica Werner, Huichen Wang, Paul Doetsch, Ya Wang

PDF file, 185K, Supplementary Table S1. Sequences of the primers used in plasmid instruction or in real-time PCR. Supplementary Figure S1. The ROS levels in miR-21 over-expressed cells. Supplementary Figure S2 The ROS levels in 5 Gy-irradiated cells. Supplementary Figure S3 IR could not further increase miR-21 levels in the cells over-expressed with miR-21. Supplementary Figure S4 The SOD levels in miR-21 over-expressed cells at different times after exposure to 5 Gy. Supplementary Figure S5 The sequence of SOD33'UTR contains a potential miR-21 binding site. Supplementary Figure S6 SOD3 activity in the cells over-expressed with SOD3. Supplementary Figure S7 The sequence of TNFa3'UTR contains a potential miR-21 binding site. Supplementary Figure S8 The SOD2 mRNA levels in the cells over-expressed with TNFa. Supplementary Figure S9 SOD activity. Supplementary Figure S10 miR-21 does not affect the levels and activities of catalase and glutathione peroxidase.

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ARTICLE ABSTRACT

MicroRNA-21 (miR-21) is an oncomir overexpressed in most human tumors in that it promotes malignant growth and progression by acting on multiple targets. Here, we broaden the impact of miR-21 in cancer by showing that it regulates the formation of reactive oxygen species (ROS) that promote tumorigenesis. Key targets of miR-21 in mediating this function were SOD3 and TNFα. We found that miR-21 inhibited the metabolism of superoxide to hydrogen peroxide, produced either by endogenous basal activities or exposure to ionizing radiation (IR), by directing attenuating SOD3 or by an indirect mechanism that limited TNFa production, thereby reducing SOD2 levels. Importantly, both effects contributed to an elevation of IR-induced cell transformation. Our findings, therefore, establish that miR-21 promotes tumorigenesis to a large extent through its regulation of cellular ROS levels. Cancer Res; 72(18); 4707–13. ©2012 AACR.

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