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Type: Artigo de periódico
Title: Ankhd1 Silencing Inhibits Stathmin 1 Activity, Cell Proliferation And Migration Of Leukemia Cells.
Author: Machado-Neto, João Agostinho
Lazarini, Mariana
Favaro, Patricia
de Melo Campos, Paula
Scopim-Ribeiro, Renata
Franchi, Gilberto Carlos
Nowill, Alexandre Eduardo
Lima, Paulo Roberto Moura
Costa, Fernando Ferreira
Benichou, Serge
Olalla Saad, Sara Teresinha
Traina, Fabiola
Abstract: ANKHD1 is highly expressed in human acute leukemia cells and potentially regulates multiple cellular functions through its ankyrin-repeat domains. In order to identify interaction partners of the ANKHD1 protein and its role in leukemia cells, we performed a yeast two-hybrid system screen and identified SIVA, a cellular protein known to be involved in proapoptotic signaling pathways. The interaction between ANKHD1 and SIVA was confirmed by co-imunoprecipitation assays. Using human leukemia cell models and lentivirus-mediated shRNA approaches, we showed that ANKHD1 and SIVA proteins have opposing effects. While it is known that SIVA silencing promotes Stathmin 1 activation, increased cell migration and xenograft tumor growth, we showed that ANKHD1 silencing leads to Stathmin 1 inactivation, reduced cell migration and xenograft tumor growth, likely through the inhibition of SIVA/Stathmin 1 association. In addition, we observed that ANKHD1 knockdown decreases cell proliferation, without modulating apoptosis of leukemia cells, while SIVA has a proapoptotic function in U937 cells, but does not modulate proliferation in vitro. Results indicate that ANKHD1 binds to SIVA and has an important role in inducing leukemia cell proliferation and migration via the Stathmin 1 pathway. ANKHD1 may be an oncogene and participate in the leukemia cell phenotype.
Subject: Ankhd1
Acute Leukemia
Cell Proliferation
Stathmin 1
Citation: Biochimica Et Biophysica Acta. v. 1853, n. 3, p. 583-593, 2015-Mar.
Rights: fechado
Identifier DOI: 10.1016/j.bbamcr.2014.12.012
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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