Evidence map›Paper›PMID 27479180›Full record

ArticleLeukemia2017

Protein kinase CK2 regulates AKT, NF-κB and STAT3 activation, stem cell viability and proliferation in acute myeloid leukemia.

L Quotti Tubi, S Canovas Nunes, A Brancalion, E Doriguzzi Breatta, S Manni, E Mandato, F Zaffino, P Macaccaro, M Carrino, K Gianesin and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 71 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

L Quotti TubiDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
S Canovas NunesDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
A BrancalionDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
E Doriguzzi BreattaDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
S ManniDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
E MandatoDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
F ZaffinoDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
P MacaccaroDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
M CarrinoDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
K GianesinDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
L TrentinDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
G BinottoDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
R ZambelloDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
G SemenzatoDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
C GurrieriDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
F PiazzaDepartment of Medicine, Division of Hematology, University of Padova, Padova, Italy.
University of Padua · ITVeneto Institute of Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase CK2 sustains acute myeloid leukemia cell growth, but its role in leukemia stem cells is largely unknown. Here, we discovered that the CK2 catalytic α and regulatory β subunits are consistently expressed in leukemia stem cells isolated from acute myeloid leukemia patients and cell lines. CK2 inactivation with the selective inhibitor CX-4945 or RNA interference induced an accumulation of leukemia stem cells in the late S-G2-M phases of the cell cycle and triggered late-onset apoptosis. As a result, leukemia stem cells displayed an increased sensitivity to the chemotherapeutic agent doxorubicin. From a molecular standpoint, CK2 blockade was associated with a downmodulation of the stem cell-regulating protein BMI-1 and a marked impairment of AKT, nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) activation, whereas FOXO3a nuclear activity was induced. Notably, combined CK2 and either NF-κB or STAT3 inhibition resulted in a superior cytotoxic effect on leukemia stem cells. This study suggests that CK2 blockade could be a rational approach to minimize the persistence of residual leukemia cells.

Indexed as

Adenosine TriphosphateAdultAgedAged, 80 and overAntineoplastic AgentsBiomarkersCasein Kinase IICell CycleCell Line, TumorCell ProliferationCell SurvivalDrug Resistance, NeoplasmFemaleForkhead Box Protein O3Gene ExpressionHumansAdenosine TriphosphateAntineoplastic AgentsBiomarkersCasein Kinase IIForkhead Box Protein O3FOXO3 protein, humanNF-kappa BPolycomb Repressive Complex 1Protein Kinase InhibitorsProto-Oncogene Proteins c-aktSTAT3 Transcription Factor

Identifiers

PMID27479180
OpenAlexW2479798035

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.