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Title: WBP2 inhibits microRNA biogenesis via interaction with the microprocessor complex
Authors: Tabatabaeian, Hossein
Lim, Shen Kiat
Chu, Tinghine
Seah, Sock Hong
Lim, Yoon Pin
Keywords: Science::Biological sciences
Issue Date: 2021
Source: Tabatabaeian, H., Lim, S. K., Chu, T., Seah, S. H. & Lim, Y. P. (2021). WBP2 inhibits microRNA biogenesis via interaction with the microprocessor complex. Life Science Alliance, 4(7), e202101038-.
Project: MOE2016-T2-2007
Journal: Life Science Alliance
Abstract: WBP2 is an emerging oncoprotein with diverse functions in breast tumorigenesis via regulating Wnt, epidermal growth factor receptor, estrogen receptor, and Hippo. Recently, evidence shows that WBP2 is tightly regulated by the components of the miRNA biogenesis machinery such as DGCR8 and Dicer via producing both WBP2's 3'UTR and coding DNA sequence-targeting miRNAs. This led us to hypothesize that WBP2 could provide a feedback loop to the biogenesis of its key upstream regulators by regulating the microprocessor complex activity. Indeed, WBP2 suppressed microprocessor activity by blocking the processing of pri-miRNAs to pre-miRNAs. WBP2 negatively regulated the assembly of the microprocessor complex via physical interactions with its components. Meta-analyses suggest that microprocessor complex components, in particular DGCR8, DDX5, and DEAD-Box Helicase17 (DDX17), have tumor-suppressive properties. 2D and 3D in vitro proliferation assays revealed that WBP2 blocked the tumor-suppressive properties of DGCR8, a key component of the microprocessor complex. In conclusion, WBP2 is a novel regulator of miRNA biogenesis that is a known dysregulated pathway in breast tumorigenesis. The reregulation of miRNA biogenesis machinery via targeting WBP2 protein may have implications in breast cancer therapy.
ISSN: 2575-1077
DOI: 10.26508/lsa.202101038
Schools: School of Biological Sciences 
Organisations: National University of Singapore
Rights: © 2021 Tabatabaeian et al. This article is available under a Creative Commons License (Attribution 4.0 International, as described at
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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