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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183844 | GEO | 2025/10/21

REPOSITORIES: GEO

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [array]

Project description:Purpose: The goals of this study are to compare the transcriptome profile of human cord blood derived CD34+ cells expressing shRNA targeting FBXO11 or non-targeting shRNA by microarray. Methods: mRNA profiles of CD34+ cord blood cells expressing non-targeting shRNA or shRNA targeting FBXO11 were generated by microarray sequencing.

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [RNA-seq]

Project description:Purpose: The goals of this study are to compare the transcriptome profile of human cord blood derived CD34+ cells expressing shRNA targeting FBXO1, LONP1 or non-targeting shRNA, combined with or without over-expression of FLAG-FBXO11 or LONP1 by RNAseq. Methods: mRNA profiles of CD34+ cord blood cells with combinations of FBXO11 or LONP1 knockdown or over-expression were generated by RNAseq.

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [array]

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PHF6 loss reduces leukemia stem cell activity in an acute myeloid leukemia mouse model.

Project description:Acute myeloid leukemia (AML) is a malignant hematologic disease caused by gene mutations and genomic rearrangements in hematologic progenitors. The PHF6 (PHD finger protein 6) gene is highly conserved and located on the X chromosome in humans and mice. We found that PHF6 was highly expressed in AML cells with MLL rearrangement and was related to the shortened survival time of AML patients. In our study, we knocked out the Phf6 gene at different disease stages in the AML mice model. Moreover, we knocked down PHF6 by shRNA in two AML cell lines and examined the cell growth, apoptosis, and cell cycle. We found that PHF6 deletion significantly inhibited the proliferation of leukemic cells and prolonged the survival time of AML mice. Interestingly, the deletion of PHF6 at a later stage of the disease displayed a better anti-leukemia effect. The expressions of genes related to cell differentiation were increased, while genes that inhibit cell differentiation were decreased with PHF6 knockout. It is very important to analyze the maintenance role of PHF6 in AML, which is different from its tumor-suppressing function in T-cell acute lymphoblastic leukemia (T-ALL). Our study showed that inhibiting PHF6 expression may be a potential therapeutic strategy targeting AML patients.

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