American Association for Cancer Research
00085472can191471-sup-221797_3_supp_5929249_q1nljx.xlsx (12.98 kB)

Table S2 from ARRB1-Promoted NOTCH1 Degradation Is Suppressed by OncomiR miR-223 in T-cell Acute Lymphoblastic Leukemia

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posted on 2023-03-31, 03:26 authored by Yi Shu, Yi Wang, Wen-Qiong Lv, Dan-Yi Peng, Juan Li, Hang Zhang, Guang-Jie Jiang, Bi-Jie Yang, Shan Liu, Jia Zhang, Yan-Hua Chen, Shi Tang, Ke-Xing Wan, Jun-Tao Yuan, Wei Guo, Guo Fu, Xin-Kun Qi, Zhi-Dai Liu, Hai-Yan Liu, Chao Yang, Ling-Huan Zhang, Fang-Jie Liu, Jie Yu, Peng-Hui Zhang, Bin Qu, Hui Zhao, Tong-Chuan He, Lin Zou

Table S2, Supplementary Table2. The characteristics of T-ALL cases


National Natural Science Foundation of China


National Key Research and Development Program of China

University of Chicago Cancer Center

National Center for Advancing Translational Sciences

Mabel Green Myers Research Endowment Fund and The University of Chicago Orthopaedics Alumni Fund.

The University of Chicago Orthopaedics Alumni Fund



T-cell acute lymphoblastic leukemia (T-ALL) is a type of aggressive leukemia with inferior prognosis. Although activating mutations of NOTCH1 are observed in most T-ALL cases, these mutations alone are not sufficient to drive the full development of T-ALL. β-Arrestins (ARRB) are versatile and multifunctional adapter proteins that regulate diverse cellular functions, including promoting the development of cancer. However, the role of ARRBs in T-ALL has largely remained elusive. In this study, we showed that ARRB1 is expressed at low levels in assayed T-ALL clinical samples and cell lines. Exogenous ARRB1 expression inhibited T-ALL proliferation and improved the survival of T-ALL xenograft animals. ARRB1 facilitated NOTCH1 ubiquitination and degradation through interactions with NOTCH1 and DTX1. Mechanistically, the oncogenic miRNA (oncomiR) miR-223 targets the 3′-UTR of ARRB1 (BUTR) and inhibits its expression in T-ALL. Furthermore, overexpression of the ARRB1-derived miR-223 sponge suppressed T-ALL cell proliferation and induced apoptosis. Collectively, these results demonstrate that ARRB1 acts as a tumor suppressor in T-ALL by promoting NOTCH1 degradation, which is inhibited by elevated miR-223, suggesting that ARRB1 may serve as a valid drug target in the development of novel T-ALL therapeutics.Significance: These findings highlight a novel tumor suppressive function of the adaptor protein β-arrestin1 in T-ALL.