| 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)
|
