Evidence map›Paper›PMID 32123842›Full record

ArticleFASEB bioAdvances2019

Kras promotes myeloid differentiation through Wnt/β-catenin signaling.

Noriko Yokoyama, Yeon-Jeong Kim, Yoshio Hirabayashi, Yoko Tabe, Kenji Takamori, Hideoki Ogawa, Kazuhisa Iwabuchi

Open access · goldAbstract read
In one paragraph

Article in FASEB bioAdvances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 9 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

7 authors at 4 institutions in 1 country.

Noriko YokoyamaInstitute for Environmental and Gender Specific Medicine Juntendo University Graduate School of Medicine Urayasu Chiba Japan.
Yeon-Jeong KimLaboratory for Neuronal Growth Mechanisms Riken Brain Science Institutes Saitama Japan.
Yoshio HirabayashiInstitute for Environmental and Gender Specific Medicine Juntendo University Graduate School of Medicine Urayasu Chiba Japan.
Yoko TabeDepartment of Laboratory Medicine Juntendo University School of Medicine Hospital Hongo Tokyo Japan.
Kenji TakamoriInstitute for Environmental and Gender Specific Medicine Juntendo University Graduate School of Medicine Urayasu Chiba Japan.
Hideoki OgawaInstitute for Environmental and Gender Specific Medicine Juntendo University Graduate School of Medicine Urayasu Chiba Japan.
Kazuhisa IwabuchiInstitute for Environmental and Gender Specific Medicine Juntendo University Graduate School of Medicine Urayasu Chiba Japan.
Juntendo University · JPJuntendo University Hospital · JPJuntendo University Urayasu Hospital · JPRIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wild-type Kras, a small GTPase, inactivates Ras growth-promoting signaling. However, the role of Kras in differentiation of myeloid cells remains unclear. This study showed the involvement of Kras in a novel regulatory mechanism underlying the dimethyl sulfoxide (DMSO)-induced differentiation of human acute myeloid leukemia HL-60 cells. Kras was found to positively regulate DMSO-induced differentiation, with the activity of Kras increasing upon DMSO. Inhibition of Kras attenuated CD11b expression in differentiated HL-60 cells. GSK3β, an important component of Wnt signaling, was found to be a downstream signal of Kras. Phosphorylation of GSK3β was markedly enhanced by DMSO treatment. Moreover, inhibition of GSK3β enhanced CD11b expression and triggered the accumulation in the nucleus of β-catenin and Tcf in response to DMSO. Inhibitors of β-catenin-mediated pathways blocked CD11b expression, further indicating that β-catenin is involved in the differentiation of HL-60 cells. Elevated expression of C/EBPα and C/EBPɛ accompanied by the expression of granulocyte colony-stimulating factor (G-CSF) receptor was observed during differentiation. Taken together, these findings suggest that Kras engages in cross talk with the Wnt/β-catenin pathway upon DMSO treatment of HL-60 cells, thereby regulating the granulocytic differentiation of HL-60 cells. These results indicate that Kras acts as a tumor suppressor during the differentiation of myeloid cells.

Indexed as

GSK3βHL‐60 cell differentiationtumor suppressorwild‐type KrasWnt/β-catenin

Identifiers

PMID32123842
PMCPMC6996383
OpenAlexW2946634843

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.