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. 2019 Sep 30;10(10):737. doi: 10.1038/s41419-019-1977-3

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© The Author(s) 2019

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 The Kaplan–Meier analysis reveals that high expression of TRIM71 moderately improves disease-free survival of ovarian cancer patients. b High expression of TRIM71 moderately improves disease-free survival of the TP53-mutated ovarian cancer patients. c High expression of TRIM71 significantly improves disease-free survival of the ovarian cancer patients sustaining TP53 mutations and low level of MDM2. d High expression of TRIM71 significantly improves disease-free survival of the ovarian cancer patients sustaining TP53 mutations and high level of HSP90. e, f The Kaplan–Meier analyses reveal that high expression of TRIM71 moderately improves disease-free survival of the TP53-mutated liver hepatocellular cancer patients f, but not the overall liver hepatocellular cancer patients e. g High expression of TRIM71 significantly improves disease-free survival of the liver hepatocellular cancer patients sustaining TP53 mutations and low level of MDM2. h High expression of TRIM71 significantly improves disease-free survival of the hepatocellular cancer patients sustaining TP53 mutations and high level of HSP90. i Overexpression of MDM2 attenuates the interaction between TRIM71 and mtp53-R273H. HCT116^p53−/− cells were transfected with combinations of plasmids encoding HA-MDM2, Myc-TRIM71, and Flag-p53-R273H followed by co-IP-IB assays using antibodies as indicated. MG132 (20 μm) was supplemented for 6 h prior to cell harvest. j, k Nutlin-3 treatment enhances j, whereas 17-AAG treatment suppresses k, the interaction between TRIM71 and mtp53-R273H. HCT116^p53−/− cells were transfected with plasmids encoding Myc-TRIM71 and Flag-p53-R273H followed by co-IP-IB assays using antibodies as indicated. Nutlin-3 (10 μm) or 17-AAG (5 μm) was supplemented for 24 h, and MG132 (20 μm) was supplemented for 6 h prior to cell harvest. l TRIM71 is unable to induce mtp53 degradation in the presence of 17-AAG. ES-2 cells infected with control or TRIM71-expressing lentiviruses were treated with or without 17-AAG (5 μm) for 24 h followed by the IB analysis using antibodies as indicated. m The working model for TRIM71’s tumor-suppressive function by inducing mtp53 degradation and consequently preventing tumor growth and metastasis