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Positive interactions between STAP-1 and BCR-ABL influence chronic myeloid leukemia cell proliferation and survival

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Title: Positive interactions between STAP-1 and BCR-ABL influence chronic myeloid leukemia cell proliferation and survival
Authors: Ishiura, Marie Browse this author
Kitai, Yuichi Browse this author →KAKEN DB
Kashiwakura, Jun-ichi Browse this author →KAKEN DB
Muromoto, Ryuta Browse this author →KAKEN DB
Toda, Jun Browse this author
Ichii, Michiko Browse this author
Oritani, Kenji Browse this author →KAKEN DB
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: CML
Issue Date: 4-Jun-2021
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 556
Start Page: 185
End Page: 191
Publisher DOI: 10.1016/j.bbrc.2021.03.162
Abstract: Chronic myeloid leukemia (CML) is a clonal disease characterized by the presence of the Philadelphia chromosome and its oncogenic product, BCR-ABL, which activates multiple pathways involved in cell survival, growth promotion, and disease progression. We recently reported that signal-transducing adaptor protein 1 (STAP-1) is upregulated in CML stem cells (LSCs) and functions to reduce the apoptosis of CML LSCs by upregulating the STAT5-downstream anti-apoptotic genes. In this study, we demonstrate the detailed molecular interactions among BCR-ABL, STAP-1, and signal transducer and activator of transcription 5 (STAT5). Studies with deletion mutants have revealed that STAP-1 interacts with BCR-ABL and STAT5a through its SH2 and PH domains, respectively, suggesting the possible role of STAP-1 as a scaffold protein. Furthermore, the binding of STAP-1 to BCR-ABL stabilizes the BCR-ABL protein in CML cells. Since STAP-1 is highly expressed in CML cells, we also analyzed the STAP-1 promoter activity using a luciferase reporter construct and found that NFATc1 is involved in activating the STAP-1 promoter and inducing STAP-1 mRNA expression. Our results demonstrate that STAP-1 contributes to the BCR-ABL/STAT5 and BCR-ABL/Ca2+/NFAT signals to induce proliferation and STAP-1 mRNA expression in CML cells, respectively.
Rights: © <2021>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

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