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HuR translocation to the cytoplasm of cancer cells in actin-independent manner

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/75223

Title: HuR translocation to the cytoplasm of cancer cells in actin-independent manner
Authors: Habiba, Umma Browse this author
Kuroshima, Takeshi Browse this author
Yanagawa-Matsuda, Aya Browse this author →KAKEN DB
Kitamura, Tetsuya Browse this author →KAKEN DB
Chowdhury, A. F. M. A. Browse this author
Jehung, Jumond P. Browse this author
Hossain, Elora Browse this author
Sano, Hidehiko Browse this author →KAKEN DB
Kitagawa, Yoshimasa Browse this author →KAKEN DB
Shindoh, Masanobu Browse this author →KAKEN DB
Higashino, Fumihiro Browse this author →KAKEN DB
Keywords: HuR, human antigen R
ARE, AU-rich element
3 '-untranslated region (3 '-UTR)
Latrunculin A (LatA)
Blebbistatin (blebbistat)
Human Angiotensin II (Ang.II)
COX-2, cyclooxygenase-2
Issue Date: 15-Aug-2018
Publisher: Elsevier
Journal Title: Experimental cell research
Volume: 369
Issue: 2
Start Page: 218
End Page: 225
Publisher DOI: 10.1016/j.yexcr.2018.05.021
Abstract: Human antigen R (HuR) is a RNA-binding protein, which binds to the AU-rich element (ARE) in the 3'-untranslated region (3'-UTR) of certain mRNA and is involved in the export and stabilization of ARE-mRNA. HuR constitutively relocates to the cytoplasm in many cancer cells, however the mechanism of intracellular HuR trafficking is poorly understood. To address this question, we examined the functional role of the cytoskeleton in HuR relocalization. We tested the effect of actin depolymerizing macrolide latrunculin A or myosin II ATPase activity inhibitor blebbistatin for HuR relocalization induced by the vasoactive hormone Angiotensin II in cancer and control normal cells. Western blot and confocal imaging data revealed that both inhibitors attenuated the cytoplasmic HuR in normal cells but no such alteration was observed in cancer cells. Concomitant with changes in intracellular HuR localization, both inhibitors markedly decreased the accumulation and half-lives of HuR target ARE-mRNAs in normal cells, whereas no change was observed in cancer cells. Furthermore, co-immunoprecipitation experiments with HuR proteins revealed clear physical interaction with beta-actin only in normal cells. The current study is the first to verify that cancer cells can implicate a microfilament independent HuR transport. We hypothesized that when cytoskeleton structure is impaired, cancer cells can acquire an alternative HuR trafficking strategy.
Rights: © 2018, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/75223
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 東野 史裕

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