p53 target gene Rap2B regulates the cytoskeleton and inhibits cell spreading

Purpose Cell migration requires spatiotemporal integration of signals that target cytoskeletal. Previous studies have indicated that Rho GTPases are crucial regulators of actin dynamics. As homologs of Rho proteins, the role of Rap2B in the regulation of cytoskeleton and its cell signaling pathway r...

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Veröffentlicht in:Journal of cancer research and clinical oncology 2015-10, Vol.141 (10), p.1791-1798
Hauptverfasser: Di, Jiehui, Huang, Hui, Wang, Yan, Qu, Debao, Tang, Juanjuan, Cheng, Qian, Lu, Zheng, Zhang, Yanping, Zheng, Junnian
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container_end_page 1798
container_issue 10
container_start_page 1791
container_title Journal of cancer research and clinical oncology
container_volume 141
creator Di, Jiehui
Huang, Hui
Wang, Yan
Qu, Debao
Tang, Juanjuan
Cheng, Qian
Lu, Zheng
Zhang, Yanping
Zheng, Junnian
description Purpose Cell migration requires spatiotemporal integration of signals that target cytoskeletal. Previous studies have indicated that Rho GTPases are crucial regulators of actin dynamics. As homologs of Rho proteins, the role of Rap2B in the regulation of cytoskeleton and its cell signaling pathway remains unknown. Methods The cellular functions of Rap2B were monitored by Western blotting and immunofluorescence staining in order to characterize the protein level and the cell shape. Results Here, we show that expression of Rap2B was induced by nocodazole in a p53-dependent manner. However, Rap2B itself is not necessary for p53-dependent cell cycle arrest. We evidenced that over-expression of Rap2B may inhibit cell spreading by disrupting actin dynamics upon nocodazole treatment, but Rap2B (C180A) mutant does not. In contrast, knockdown of Rap2B promoted cell spreading. Conclusions Altogether, these results revealed that Rap2B plays a pivotal role in cytoskeleton reorganization and subsequently inhibits cell spreading, which could be responsible for cancer metastasis.
doi_str_mv 10.1007/s00432-015-1948-8
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Previous studies have indicated that Rho GTPases are crucial regulators of actin dynamics. As homologs of Rho proteins, the role of Rap2B in the regulation of cytoskeleton and its cell signaling pathway remains unknown. Methods The cellular functions of Rap2B were monitored by Western blotting and immunofluorescence staining in order to characterize the protein level and the cell shape. Results Here, we show that expression of Rap2B was induced by nocodazole in a p53-dependent manner. However, Rap2B itself is not necessary for p53-dependent cell cycle arrest. We evidenced that over-expression of Rap2B may inhibit cell spreading by disrupting actin dynamics upon nocodazole treatment, but Rap2B (C180A) mutant does not. In contrast, knockdown of Rap2B promoted cell spreading. Conclusions Altogether, these results revealed that Rap2B plays a pivotal role in cytoskeleton reorganization and subsequently inhibits cell spreading, which could be responsible for cancer metastasis.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-015-1948-8</identifier><identifier>PMID: 25762091</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Actins - metabolism ; Cancer ; Cancer Research ; Cell Cycle Checkpoints - physiology ; Cell Line, Tumor ; Cell Movement - physiology ; Cytoskeleton ; Cytoskeleton - metabolism ; Cytoskeleton - pathology ; Genes ; Hematology ; Humans ; Internal Medicine ; Medicine ; Medicine &amp; Public Health ; Oncology ; Original Article – Cancer Research ; Proteins ; rap GTP-Binding Proteins - metabolism ; rho GTP-Binding Proteins - metabolism ; Signal Transduction - physiology ; Studies ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Journal of cancer research and clinical oncology, 2015-10, Vol.141 (10), p.1791-1798</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-47c4437b7e9bef71b2799e83b760a6bb42d06492162af11fea104552a5765af83</citedby><cites>FETCH-LOGICAL-c475t-47c4437b7e9bef71b2799e83b760a6bb42d06492162af11fea104552a5765af83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-015-1948-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-015-1948-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25762091$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Di, Jiehui</creatorcontrib><creatorcontrib>Huang, Hui</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Qu, Debao</creatorcontrib><creatorcontrib>Tang, Juanjuan</creatorcontrib><creatorcontrib>Cheng, Qian</creatorcontrib><creatorcontrib>Lu, Zheng</creatorcontrib><creatorcontrib>Zhang, Yanping</creatorcontrib><creatorcontrib>Zheng, Junnian</creatorcontrib><title>p53 target gene Rap2B regulates the cytoskeleton and inhibits cell spreading</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose Cell migration requires spatiotemporal integration of signals that target cytoskeletal. 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Previous studies have indicated that Rho GTPases are crucial regulators of actin dynamics. As homologs of Rho proteins, the role of Rap2B in the regulation of cytoskeleton and its cell signaling pathway remains unknown. Methods The cellular functions of Rap2B were monitored by Western blotting and immunofluorescence staining in order to characterize the protein level and the cell shape. Results Here, we show that expression of Rap2B was induced by nocodazole in a p53-dependent manner. However, Rap2B itself is not necessary for p53-dependent cell cycle arrest. We evidenced that over-expression of Rap2B may inhibit cell spreading by disrupting actin dynamics upon nocodazole treatment, but Rap2B (C180A) mutant does not. In contrast, knockdown of Rap2B promoted cell spreading. 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subjects Actins - metabolism
Cancer
Cancer Research
Cell Cycle Checkpoints - physiology
Cell Line, Tumor
Cell Movement - physiology
Cytoskeleton
Cytoskeleton - metabolism
Cytoskeleton - pathology
Genes
Hematology
Humans
Internal Medicine
Medicine
Medicine & Public Health
Oncology
Original Article – Cancer Research
Proteins
rap GTP-Binding Proteins - metabolism
rho GTP-Binding Proteins - metabolism
Signal Transduction - physiology
Studies
Tumor Suppressor Protein p53 - metabolism
title p53 target gene Rap2B regulates the cytoskeleton and inhibits cell spreading
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