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Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

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CITED2 affects leukemic cell survival by interfering with p53 activation.

Katharina Mattes¹, Gerbrig Berger¹, Marjan Geugien¹

¹Department of Hematology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

Cell Death & Disease

|October 27, 2017

Summary

CITED2 (CBP/p300-interacting-transactivator-with-an-ED-rich-tail 2) knockdown in acute myeloid leukemia (AML) cells prolonged mouse survival. Reduced CITED2 activated p53, inhibited AKT signaling, and decreased MDM2 interaction, offering a potential AML therapeutic target.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53

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Published on: August 4, 2019

Area of Science:

Molecular Biology
Cancer Research
Hematology

Background:

CITED2 (CBP/p300-interacting-transactivator-with-an-ED-rich-tail 2) is implicated in acute myeloid leukemia (AML).
Elevated CITED2 levels are observed in certain AML cases.
The role of CITED2 in AML pathogenesis requires further investigation.

Purpose of the Study:

To elucidate the in vivo function of CITED2 in maintaining AML.
To investigate the molecular mechanisms underlying CITED2's role in AML.
To assess CITED2 as a potential therapeutic target for AML.

Main Methods:

Lentiviral RNA interference (RNAi) for CITED2 knockdown in AML cells.
In vivo studies using mouse transplantation models with CITED2-knockdown AML cells.
In vitro analyses of apoptosis, signaling pathways (p53, AKT, CBP/p300), and protein interactions (p53-MDM2).

Main Results:

CITED2 knockdown in AML cells significantly increased survival in transplanted mice.
Reduced CITED2 induced p53-mediated apoptosis, increased CDKN1A, and decreased BCL2.
CITED2 loss inhibited AKT signaling and decreased p53-MDM2 interaction, leading to increased p53 levels.

Conclusions:

CITED2 plays a crucial role in AML maintenance by regulating p53 activity and AKT signaling.
CITED2 knockdown promotes apoptosis and extends survival in AML models.
CITED2 represents a promising therapeutic target for AML, particularly in cases with p53 pathway inactivation.