Evidence map›Paper›PMID 33074481›Full record

ArticleInternational journal of hematology2021

Salt-inducible kinase inhibition sensitizes human acute myeloid leukemia cells to all-trans retinoic acid-induced differentiation.

Xue-Wen Zhang, Xing Shen, Wen-Yue Long, He Xiao, Feng-Jun Li, Shuang Xing, Guo-Lin Xiong, Zu-Yin Yu, Yu-Wen Cong

Abstract read
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In one paragraph

Article in International journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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 2 institutions in 1 country.

Xue-Wen Zhang *Guangdong Pharmaceutical University, Guangzhou, China.
Xing Shen *Department of Experimental Hematology and Biochemistry, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.
Wen-Yue LongDepartment of Experimental Hematology and Biochemistry, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.
He XiaoDepartment of Molecular Immunology, Institute of Pharmacology and Toxicology, Beijing, China.
Feng-Jun LiDepartment of Experimental Hematology and Biochemistry, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.
Shuang XingDepartment of Experimental Hematology and Biochemistry, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.
Guo-Lin XiongDepartment of Experimental Hematology and Biochemistry, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.
Zu-Yin YuGuangdong Pharmaceutical University, Guangzhou, China. yuzy79@163.com.ORCID http://orcid.org/0000-0001-7037-4479
Yu-Wen CongGuangdong Pharmaceutical University, Guangzhou, China. congyw@bmi.ac.cn.
Beijing Radiation Center · CNGuangdong Pharmaceutical University · CN

Funding

The National Natural Science Foundation of China (CN) 81273544
6 · The paper itself

Abstract

Differentiation therapies with all-trans retinoic acid (ATRA) have been successful in treating acute promyelocytic leukemia, a rare subtype of acute myeloid leukemia (AML). However, their efficacy is limited in the case of other AML subtypes. Here, we show that the combination of ATRA with salt-inducible kinase (SIK) inhibition significantly enhances ATRA-mediated AML differentiation. SIK inhibition augmented the ability of ATRA to induce growth inhibition and G1 cell cycle arrest of AML cells. Moreover, combining ATRA and SIK inhibition synergistically activated the Akt signaling pathway but not the MAPK pathway. Pharmacological blockade of Akt activity suppressed the combination-induced differentiation, indicating an essential role for Akt in the action of the combination treatment. Taken together, our study reveals a novel role for SIK in the regulation of ATRA-mediated AML differentiation, implicating the combination of ATRA and SIK inhibition as a promising approach for future differentiation therapy.

Indexed as

Antineoplastic AgentsApoptosisBiomarkersCell CycleCell DifferentiationCell Line, TumorDrug Resistance, NeoplasmHumansImmunohistochemistryImmunophenotypingLeukemia, Myeloid, AcuteMAP Kinase Signaling SystemProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTretinoinAntineoplastic AgentsBiomarkersProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSIK1 protein, humanTretinoinAcute myeloid leukemiaAktATRADifferentiationSalt-inducible kinase

Identifiers

PMID33074481
OpenAlexW3093388198

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.