miR-155 expression and function in leukemic stem cells

2024 · doi:10.1101/2024.02.29.582835
preprint OA: closed CC-BY-NC-ND-4.0
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The paper studied how miR-155 is expressed in clearly defined leukemic stem cell (LSC) populations and tested whether miR-155 regulates LSC function in acute myeloid leukemia (AML). The authors found that miR-155 is regulating LSC self-renewal and quiescence, clarifying its potential role in maintaining LSC properties, while noting prior reports that elevated miR-155 in FLT3-ITD AML can be independent of FLT3-ITD signaling. A limitation explicitly stated in the provided text is that the study was addressing an existing uncertainty about LCS-specific expression and function rather than evaluating related clinical contexts in the abstract. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

ABSTRACT It has been reported that elevated levels of miR-155 have been reported in patients with Acute Myeloid Leukemia (AML) bearing FLT3 -ITD mutations and is independent of FLT3 -ITD signaling. However, it is unclear how miR-155 is expressed in leukemic stem cells (LCS) and whether miR-155 has any role regulating LSC functions. In this manuscript, we defined the expression of miR-155 in clearly defined LCSs population and showed that miR-155 is regulating self-renewal and quiescence of LSCs.
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ABSTRACT It has been reported that elevated levels of miR-155 have been reported in patients with Acute Myeloid Leukemia (AML) bearing FLT3-ITD mutations and is independent of FLT3-ITD signaling. However, it is unclear how miR-155 is expressed in leukemic stem cells (LCS) and whether miR-155 has any role regulating LSC functions. In this manuscript, we defined the expression of miR-155 in clearly defined LCSs population and showed that miR-155 is regulating self-renewal and quiescence of LSCs. Competing Interest Statement The authors have declared no competing interest. Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.

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License: CC-BY-NC-ND-4.0