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The clinical significance of γ-catenin in acute myeloid leukemia

Authors Xu J, Wu W, Shen W, Liu P

Received 1 February 2016

Accepted for publication 26 April 2016

Published 27 June 2016 Volume 2016:9 Pages 3861—3871

DOI https://doi.org/10.2147/OTT.S105514

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Triparna Sen

Peer reviewer comments 2

Editor who approved publication: Dr William Cho


Jiadai Xu,1 Wei Wu,1 Wenyi Shen,1 Peng Liu2

1Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 2Department of Hematology, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China

Abstract: Dysregulation of γ-catenin may function as an oncogenic factor in various malignancies. We investigated γ-catenin expression in acute myeloid leukemia (AML) and explored its role in the pathogenesis of AML. γ-Catenin was significantly overexpressed in AML patients compared to healthy donors. The γ-catenin expression in AML patients with lower white blood cells (<30×109/L) was significantly higher than those with higher white blood cells (≥30×109/L). The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα. AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels. In K562 cells, γ-catenin knockdown suppressed cellular proliferation, while the cellular migration was greatly enhanced. Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells. Our investigation has indicated a potential role of γ-catenin in the pathogenesis of AML.

Keywords: γ-catenin, acute myeloid leukemia, AML, decitabine, prognosis, bone marrow, shRNA

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