Jul 1, 2018 · RNA-seq analysis reveals changes in CDKN1A and CDKN2B-mediated gene expression, altering the AML transcriptome in ways that facilitate cell cycle arrest.

Nov 15, 2022 · CDKN1A is involved in p53/TP53 mediated inhibition of cellular proliferation in response to DNA damage. Both were down-regulated in AML patients and are likely to play an important role in the pathogenesis of AML.

Aug 1, 2024 · Our chromatin mapping analysis in AML cell lines identified two unreported enhancers near CDKN1A gene where the Chromatin Assembly Factor 1 (CAF1) complex, a master epigenetic regulator of leukemia cell fate, and the pro-myeloid transcription factor CEBPA exhibited antagonistic binding profile.

Nov 8, 2022 · Here, we demonstrate that tumor cell phagocytosis drives the pro-inflammatory activation of TAMs and identify a key role for the cyclin-dependent kinase inhibitor CDKN1A (p21).

Jun 6, 2024 · Utilizing de novo AML patient and control samples we studied the expression of PPP1R15A, CDKN1A, GADD45A, GADD45G, and EXO1. Next, we performed PPP1R15A silencing in AML cell lines in two separate experiments using …

TWIST1 overexpression increased methylation levels of promoter areas of CDKN1A/C in cell lines and primary cells. CDKN1A/C are CDK inhibitors that strongly affect various G1 cyclin/CDK complexes and thereby negatively regulate cell proliferation.

Apr 23, 2015 · We observed that decitabine treatment increased CDKN1A and FOXO3A expression levels at both the RNA and protein level in the AML cell lines OCI-AML3, MV4-11, and MOLM-13 (Figure 1C and supplemental Figure 2B), which supports this hypothesis.

APTO-253 is a phase I clinical stage small molecule that selectively induces CDKN1A (p21), promotes G₀-G₁ cell-cycle arrest, and triggers apoptosis in acute myeloid leukemia (AML) cells without producing myelosuppression in various animal species and …

CDKN1A, ERCC1, PARP1 and BAP1 misregulation is validated in an independent CMML cohort and their behaviour through myeloid disorders replicated by both direct and global comprehensive techniques.

To confirm p53 activation by MDM2 inhibition we determined the expression levels of the tumor suppressor protein p53, of the activated acetylated p53 protein and of the p53 target gene CDKN1A in AML cells treated for 24 h with single compounds and with combined treatment.