Evidence map›Paper›PMID 33130330›Full record

ArticleLeukemia research2020

Evidence that knock down of GSK-3β in Chronic Myelogenous Leukemia cells augments IFN-γ-induced apoptosis.

Melissa R Kauffman, Saeed Nazemidashtarjandi, Davoud Ghazanfari, Abigail E Allen, Nathan M Reynolds, Ahmed Faik, Monica M Burdick, Kelly D McCall, Douglas J Goetz

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Resolvin D2 restores monocyte anisocytosis and mediates a shift toward classical monocytes ex vivo in blood samples from patients after major burns.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  2. HAP1, a new revolutionary cell model for gene editing using CRISPR-Cas9.Frontiers in cell and developmental biology · 2023
    Review
  3. Review
  4. Article
  5. Article
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

9 authors at 1 institution in 1 country.

Melissa R KauffmanDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA; Biomedical Engineering Program, Ohio University, Athens, OH 45701, USA.
Saeed NazemidashtarjandiDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA.
Davoud GhazanfariDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA.
Abigail E AllenDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA; Biomedical Engineering Program, Ohio University, Athens, OH 45701, USA.
Nathan M ReynoldsDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA; Translational Biomedical Sciences Program, Ohio University, Athens, OH 45701, USA.
Ahmed FaikEnvironmental and Plant Biology Department, Ohio University, Athens, OH 45701, USA; Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA.
Monica M BurdickDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA; Biomedical Engineering Program, Ohio University, Athens, OH 45701, USA; Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA; Translational Biomedical Sciences Program, Ohio University, Athens, OH 45701, USA.
Kelly D McCallBiomedical Engineering Program, Ohio University, Athens, OH 45701, USA; Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA; Translational Biomedical Sciences Program, Ohio University, Athens, OH 45701, USA; Department of Specialty Medicine, Ohio University, Athens, OH 45701, USA; The Diabetes Institute, Ohio University, Athens, OH 45701, USA.
Douglas J GoetzDepartment of Chemical and Biomolecular Engineering, Ohio University, Athens, OH 45701, USA; Biomedical Engineering Program, Ohio University, Athens, OH 45701, USA; Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA; Translational Biomedical Sciences Program, Ohio University, Athens, OH 45701, USA. Electronic address: goetzd@ohio.edu.
Ohio University · US

Funding

Cardiovascular Bioengineering Training ProgramT32HL076124 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANJEEV G SHROFF · 2005 to 2026
$7.0M
Novel Glycogen Synthase Kinase-3 (GSK-3) Inhibitors as Therapeutic AgentsR15GM110602 · NIGMS · OHIO UNIVERSITY ATHENS · PI GOETZ, DOUGLAS J · 2016 to 2025
$1.5M
NHLBI NIH HHS T32 HL076124NIGMS NIH HHS R15 GM110602
6 · The paper itself

Abstract

The role of interferon-gamma (IFN-γ) in Chronic Myelogenous/Myeloid Leukemia (CML) and in the treatment of CML remains unclear; specifically, the effect of IFN-γ on apoptosis. There is reported interplay between IFN-γ and glycogen synthase kinase-3 (GSK-3), a kinase which has been implicated in both cell death and, conversely, cell survival. Thus, we utilized the CML-derived HAP1 cell line and a mutant HAP1 GSK-3β knocked-down cell line (GSK-3β 31bp) to investigate whether GSK-3 modulates IFN-γ's action on CML cells. Significantly less GSK-3β 31bp cells, relative to HAP1 cells, were present after 48 h treatment with IFN-γ. IFN-γ treatment significantly decreased GSK-3β 31bp substrate adhesiveness (relative to HAP1 cells); an observation often correlated with cell death. Fluorescence microscopy revealed that IFN-γ induces a modest level of apoptosis in the HAP1 cells and that IFN-γ induced apoptosis is significantly enhanced in GSK-3β 31bp cells. Utilizing a complementary GSK-3β knocked-down cell line (8bp) we found, via flow cytometric analysis, that IFN-γ induced apoptosis is significantly enhanced in GSK-3β 8bp cells relative to HAP1 cells. Combined, our findings suggest that IFN-γ induces apoptosis of CML cells and that loss of GSK-3β significantly augments IFN-γ-induced apoptosis.

Indexed as

Antineoplastic AgentsApoptosisCell AdhesionCell Line, TumorCodon, NonsenseCRISPR-Cas SystemsDrug InteractionsFlow CytometryFrameshift MutationFusion Proteins, bcr-ablGene Knockdown TechniquesGlycogen Synthase Kinase 3 betaHumansInterferon-gammaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleAntineoplastic AgentsCodon, NonsenseFusion Proteins, bcr-ablGlycogen Synthase Kinase 3 betaIFNG protein, humanInterferon-gammaNeoplasm ProteinsProtein Kinase InhibitorsRNA, Guide, CRISPR-Cas SystemsApoptosisBCR-ABLGlycogen synthase kinase-3InterferonLeukemiaPhiladelphia chromosome

Identifiers

PMID33130330
PMCPMC7740760
OpenAlexW3094142652

What OpenQuestion holds

Textmetadata
LicenceTDM
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.