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RSPO2 inhibits BMP signaling to promote self-renewal in acute myeloid leukemia.
Cell Rep. 36:109559 (2021)
Acute myeloid leukemia (AML) is a rapidly progressing cancer, for which chemotherapy remains standard treatment and additional therapeutic targets are requisite. Here, we show that AML cells secrete the stem cell growth factor R-spondin 2 (RSPO2) to promote their self-renewal and prevent cell differentiation. Although RSPO2 is a well-known WNT agonist, we reveal that it maintains AML self-renewal WNT independently, by inhibiting BMP receptor signaling. Autocrine RSPO2 signaling is also required to prevent differentiation and to promote self-renewal in normal hematopoietic stem cells as well as primary AML cells. Comprehensive datamining reveals that RSPO2 expression is elevated in patients with AML of poor prognosis. Consistently, inhibiting RSPO2 prolongs survival in AML mouse xenograft models. Our study indicates that in AML, RSPO2 acts as an autocrine BMP antagonist to promote cancer cell renewal and may serve as a marker for poor prognosis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Acute Myeloid Leukemia ; Bmp ; Drug Resistance ; Hspc ; Leukemia Stem Cell ; Macrophages ; Monocytes ; R-spondin ; Self-renewal ; Wnt; Acute Myelogenous Leukemia; Hematopoietic Stem-cells; Wnt/beta-catenin; Wnt; Gene; Differentiation; Expression; Proteins; Cancer; Receptor
ISSN (print) / ISBN
2211-1247
e-ISSN
2211-1247
Journal
Cell Reports
Quellenangaben
Volume: 36,
Issue: 7,
Article Number: 109559
Publisher
Cell Press
Publishing Place
50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Research Unit Apoptosis in Hematopoietic Stem Cells (AHS)
Grants
Deutsche Forschungsgemeinschaft (DFG)
Max-Eder Grant of the German Cancer Aid
Deutsche Forschungsgemeinschaft
Max-Eder Grant of the German Cancer Aid
Deutsche Forschungsgemeinschaft