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TET2-mediated mRNA in leukemia stemness maintanence and homing

ABSTRACT: TET2-mediated mRNA in leukemia stemness maintanence and homing

PROVIDER: PRJNA963773 | ENA |

REPOSITORIES: ENA

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TET2-mediated mRNA in leukemia stemness maintanence and homing [RNA-Seq]

Project description:TET2-mediated mRNA in leukemia stemness maintanence and homing [RNA-Seq]

| PRJNA963840 | ENA

TET2-mediated mRNA in leukemia stemness maintanence and homing [RNA-Seq]

Project description:To assess the potential effect of Tet2 on RNA stability, mRNA half-life profiling was performed on samples enriched from AML cells with Tet2+/+ or Tet2-/- genotypes, following treatment with actinomycin D at different time points.

2023-06-22 | GSE231327 | GEO

TET2-mediated mRNA in leukemia stemness maintanence and homing

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-22 | GSE231330 | GEO

TET2-mediated mRNA demethylation regulates leukemia stem cell homing and self-renewal.

Project description:TET2 is recurrently mutated in acute myeloid leukemia (AML) and its deficiency promotes leukemogenesis (driven by aggressive oncogenic mutations) and enhances leukemia stem cell (LSC) self-renewal. However, the underlying cellular/molecular mechanisms have yet to be fully understood. Here, we show that Tet2 deficiency significantly facilitates leukemogenesis in various AML models (mediated by aggressive or less aggressive mutations) through promoting homing of LSCs into bone marrow (BM) niche to increase their self-renewal/proliferation. TET2 deficiency in AML blast cells increases expression of Tetraspanin 13 (TSPAN13) and thereby activates the CXCR4/CXCL12 signaling, leading to increased homing/migration of LSCs into BM niche. Mechanistically, TET2 deficiency results in the accumulation of methyl-5-cytosine (m5C) modification in TSPAN13 mRNA; YBX1 specifically recognizes the m5C modification and increases the stability and expression of TSPAN13 transcripts. Collectively, our studies reveal the functional importance of TET2 in leukemogenesis, leukemic blast cell migration/homing, and LSC self-renewal as an mRNA m5C demethylase.

| S-EPMC11166201 | biostudies-literature

TET2-mediated mRNA in tumor immunity [m5C]

Project description:To investigate the function of TET2 as an mRNA m5C demethylase in the development of acute myeloid leukemia (AML), we conducted RNA bisulfite sequencing of mRNA samples enriched from AML cells carrying Tet2+/+ versus Tet2-/- with actinomycin D treatment at different time point.

2023-06-23 | GSE231329 | GEO

LAMP5-AS1 drives leukemia cell stemness in MLL leukemia

Project description:LAMP5-AS1 drives leukemia cell stemness in MLL leukemia

| PRJNA632553 | ENA

TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

Project description:To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

2023-06-23 | GSE206456 | GEO

TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

2023-06-23 | GSE206457 | GEO

Context Dependent Effects of Ascorbic Acid Treatment in TET2 Mutant Myeloid Neoplasia

Project description:Loss-of-function TET2 mutations (TET2MT) are common in myeloid neoplasia. TET2, a DNA dioxygenase, requires 2-oxoglutarate and Fe(II) to oxidize 5-methylcytosine. TET2MT thus result in hypermethylation and transcriptional repression. Ascorbic acid (AA) increases dioxygenase activity by facilitating Fe(III)/Fe(II) redox reaction and may alleviate some biological consequences of TET2MT by restoring dioxygenase activity. Here, we report the utility of AA in the prevention of TET2MT MN, clarify the mechanistic underpinning of the TET2-AA interactions, and demonstrate that the ability of AA to restore TET2 activity in cells depends on N- and C-terminal lysine acetylation and nature of TET2MT. Consequently, pharmacologic modulation of acetyltransferases and histone deacetylases may regulate TET dioxygenase-dependent AA effects. Thus, our study highlights the contribution of factors that may enhance or attenuate AA effects on TET2 and provides a rationale for novel therapeutic approaches including combinations of AA with class I/II HDAC inhibitor or sirtuin activators in TET2MT leukemia.

2020-09-09 | PXD020550 | Pride

NAT10-mediated mRNA N4-acetylcitidine (ac4C) Promotes Stemness and Leukemogenesis in Acute Myeloid Leukemia

Project description:NAT10-mediated mRNA N4-acetylcitidine (ac4C) Promotes Stemness and Leukemogenesis in Acute Myeloid Leukemia

| PRJNA1033527 | ENA