Evidence map›Paper›PMID 34967577›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2021

Thymoquinone Induces Downregulation of BCR-ABL/JAK/STAT Pathway and Apoptosis in K562 Leukemia Cells.

Futoon Abedrabbu Al-Rawashde, Wan Rohani Wan Taib, Imilia Ismail, Muhammad Farid Johan, Abdullah Saleh Al-Wajeeh, Hamid Ali Nagi Al-Jamal

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Epigenetic Reactivation of <italic>SOCS-3</italic> and Inhibition of ERK1/2 Underlie Thymoquinone-Induced Apoptosis in a Chronic Myeloid Leukemia Xenograft Model.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026
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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

6 authors at 3 institutions in 2 countries.

Futoon Abedrabbu Al-RawashdeSchool of Biomedicine, Faculty of Health Sciences, Universiti Sultan Zainal Abidin (UniSZA), Terengganu 21300, Malaysia.
Wan Rohani Wan TaibSchool of Biomedicine, Faculty of Health Sciences, Universiti Sultan Zainal Abidin (UniSZA), Terengganu 21300, Malaysia.
Imilia IsmailSchool of Biomedicine, Faculty of Health Sciences, Universiti Sultan Zainal Abidin (UniSZA), Terengganu 21300, Malaysia.ORCID 0000-0002-3701-4006
Muhammad Farid JohanDepartment of Haematology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia.ORCID 0000-0001-6344-0220
Abdullah Saleh Al-WajeehAnti-Doping Lab Qatar, Doha, Qatar.
Hamid Ali Nagi Al-JamalSchool of Biomedicine, Faculty of Health Sciences, Universiti Sultan Zainal Abidin (UniSZA), Terengganu 21300, Malaysia.ORCID 0000-0001-6194-2729
Sultan Zainal Abidin University · MYAnti-Doping Laboratory · QAUniversiti Sains Malaysia · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBCR ABL oncogene encodes the BCR-ABL chimeric protein, which is a constitutively activated non-receptor tyrosine kinase. The BCR-ABL oncoprotein is a key molecular basis for the pathogenesis of chronic myeloid leukemia (CML) via activation of several downstream signaling pathways including JAK/STAT pathway. Development of leukemia involves constitutive activation of signaling molecules including, JAK2, STAT3, STAT5A and STAT5B. Thymoquinone (TQ) is a bioactive constituent of Nigella sativa that has shown anticancer properties in various cancers. The present study aimed to evaluate the effect of TQ on the expression of BCR ABL, JAK2, STAT3, STAT5A and STAT5B genes and their consequences on the cell proliferation and apoptosis in K562 CML cells.

methodsBCR-ABL positive K562 CML cells were treated with TQ. Cytotoxicity was determined by Trypan blue exclusion assay. Apoptosis assay was performed by annexin V-FITC/PI staining assay and analyzed by flow cytometry. Transcription levels of BCR ABL, JAK2, STAT3, STAT5A and STAT5B genes were evaluated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Protein levels of JAK2 and STAT5 were determined by Jess Assay analysis.

resultsTQ markedly decreased the cell proliferation and induced apoptosis in K562 cells (P < 0.001) in a concentration dependent manner. TQ caused a significant decrease in the transcriptional levels of BCR ABL, JAK2, STAT3, STAT5A and STAT5B genes (P < 0.001). TQ induced a significant decrease in JAK2 and STAT5 protein levels (P < 0.001).

conclusionour results indicated that TQ inhibited cell growth of K562 cells via downregulation of BCR ABL/ JAK2/STAT3 and STAT5 signaling and reducing JAK2 and STAT5 protein levels.

Indexed as

Antineoplastic AgentsApoptosisBenzoquinonesDown-RegulationGene Expression Regulation, NeoplasticGenes, ablHumansJanus Kinase 2K562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveSignal TransductionSTAT3 Transcription FactorSTAT5 Transcription FactorTumor Suppressor ProteinsAntineoplastic AgentsBenzoquinonesJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription FactorSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorthymoquinoneTumor Suppressor ProteinsApoptosisBCR-ABLCMLSTATthymoquinone

Identifiers

PMID34967577
PMCPMC9080382
OpenAlexW4200616222

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.