Int J Med Sci 2022; 19(2):274-285. doi:10.7150/ijms.67436 This issue

Research Paper

ZFP91 promotes cell proliferation and inhibits cell apoptosis in AML via inhibiting the proteasome-dependent degradation of RIP1

Zhonghui Zhang1, Liang Zhong2, Wenran Dan1, Xuan Chu1, Chen Liu2, Xu Luo1, Peng Wan1, Zhenyan Liu1, Yang Lu1, Xiao Wang1, Beizhong Liu1,2,✉

1. Central Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China
2. Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China

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Citation:
Zhang Z, Zhong L, Dan W, Chu X, Liu C, Luo X, Wan P, Liu Z, Lu Y, Wang X, Liu B. ZFP91 promotes cell proliferation and inhibits cell apoptosis in AML via inhibiting the proteasome-dependent degradation of RIP1. Int J Med Sci 2022; 19(2):274-285. doi:10.7150/ijms.67436. Available from https://www.medsci.org/v19p0274.htm

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Abstract

Graphic abstract

Acute myeloid leukemia (AML) is a quickly progressive and devastated hematological malignancy with large rate of relapse and the appearance of chemotherapy resistance. Therefore, the identification of new therapeutic targets is urgent. ZFP91 is a hidden oncogene. Nevertheless, how ZFP91 takes part in regulating AML is less clear. Our research aims at investigating the molecular mechanisms and uncovering the effects of ZFP91 on AML. This research demonstrates that ZFP91 boosts AML cell proliferation and stops AML cell apoptosis. Mechanistically, experimental results showed the interaction between ZFP91 and RIP1 and inhibitory effect of ZFP91 on the K48-linked ubiquitination of endogenous RIP1, which is an important molecule in AML. Taken together, our results provide the evidence that targeted inhibition of ZFP91 could be a hopeful measure to treat AML.

Keywords: ZFP91, RIP1, E3 ligase, Ubiquitination, AML, Proteasome degradation