American Association for Cancer Research
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Suppl. Tables and Suppl. figure legends from Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

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journal contribution
posted on 2023-03-31, 20:09 authored by Qinghai Zeng, Jianye Liu, Peiguo Cao, Jingjing Li, Xiaoming Liu, Xiaojun Fan, Ling Liu, Yan Cheng, Wei Xiong, Jigang Li, Hao Bo, Yuxing Zhu, Fei Yang, Jun Hu, Ming Zhou, Yanhong Zhou, Qiong Zou, Jianda Zhou, Ke Cao

Suppl. Table 1: Univariate analysis of different prognostic parameters in 112 patients with BUC. Suppl. Table 2. Multivariate cox regression analysis of the association of various clinicopathological features with survival in 112 patients with BUC. Suppl. figure 1-7 legends


National Natural Science Foundation of China

Natural Science Foundation of Hunan Province

Central South University

Huxiang Young Talent Project

Third Xiangya Hospital of Central South University



Purpose: Regulated in development and DNA damage response-1 (REDD1) is a stress-related protein and is involved in the progression of cancer. The role and regulatory mechanism of REDD1 in bladder urothelial carcinoma (BUC), however, is yet unidentified.Experimental Design: The expression of REDD1 in BUC was detected by Western blot analysis and immunohistochemistry (IHC). The correlation between REDD1 expression and clinical features in patients with BUC were assessed. The effects of REDD1 on cellular proliferation, apoptosis, autophagy, and paclitaxel sensitivity were determined both in vitro and in vivo. Then the targeted-regulating mechanism of REDD1 by miRNAs was explored.Results: Here the significant increase of REDD1 expression is detected in BUC tissue, and REDD1 is first reported as an independent prognostic factor in patients with BUC. Silencing REDD1 expression in T24 and EJ cells decreased cell proliferation, increased apoptosis, and decreased autophagy, whereas the ectopic expression of REDD1 in RT4 and BIU87 cells had the opposite effect. In addition, the REDD1-mediated proliferation, apoptosis, and autophagy are found to be negatively regulated by miR-22 in vitro, which intensify the paclitaxel sensitivity via inhibition of the well-acknowledged REDD1–EEF2K–autophagy axis. AKT/mTOR signaling initially activated or inhibited in response to silencing or enhancing REDD1 expression and then recovered rapidly. Finally, the inhibited REDD1 expression by either RNAi or miR-22 sensitizes BUC tumor cells to paclitaxel in a subcutaneous transplant carcinoma model in vivo.Conclusions: REDD1 is confirmed as an oncogene in BUC, and antagonizing REDD1 could be a potential therapeutic strategy to sensitize BUC cells to paclitaxel. Clin Cancer Res; 24(2); 445–59. ©2017 AACR.

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