Evidence map›Paper›PMID 32124958›Full record

ArticleInternational journal of oncology2020

Diallyl disulfide induces downregulation and inactivation of cofilin 1 differentiation via the Rac1/ROCK1/LIMK1 pathway in leukemia cells.

Hui Ling, Xiaoxia Ji, Yanping Lei, Yanhong Jia, Fang Liu, Hong Xia, Hui Tan, Xi Zeng, Lan Yi, Jie He and 1 more

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

Article in International journal of oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
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  10. Gastrokine 2 Regulates the Antitumor Effect of JAK2/STAT3 Pathway in Gastric Cancer.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  11. 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

11 authors at 1 institution in 1 country.

Hui Ling *Key Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Xiaoxia Ji *Key Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Yanping Lei *Key Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Yanhong JiaKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Fang LiuKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Hong XiaKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Hui TanKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Xi ZengKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Lan YiKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Jie HeKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Qi SuKey Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cofilin is associated with cell differentiation; however, to the best of our knowledge, no data have indicated an association between the cofilin 1 pathway and leukemia cell differentiation. The present study investigated the involvement of the cofilin 1 signaling pathway in diallyl disulfide (DADS)‑induced differentiation and the inhibitory effects on the proliferation, migration, and invasion of human leukemia HL‑60 cells. First, it was identified that 8 µM DADS suppressed cell proliferation, migration and invasion, and induced differentiation based on the reduced nitroblue tetrazolium ability and increased CD11b and CD33 expression. DADS significantly downregulated the expression of cofilin 1 and phosphorylated cofilin 1 in HL‑60 leukemia cells. Second, it was verified that silencing cofilin 1 markedly promoted 8 µM DADS‑induced differentiation and the inhibitory effect on cell proliferation and invasion. Overexpression of cofilin 1 obviously suppressed 8 µM DADS‑induced differentiation and the inhibitory effect on cell proliferation and invasion. Third, the present study examined the mechanisms by which 8 µM DADS decreases cofilin 1 expression and activation. The results revealed that 8 µM DADS inhibited the mRNA and protein expression of Rac1, Rho‑associated protein kinase 1 (ROCK1) and LIM domain kinase 1 (LIMK1) as well as the phosphorylation of LIMK1 in HL‑60 cells, while 8 µM DADS enhanced the effects of the Rac1‑ROCK1‑LIMK1 pathway in cells overexpressing cofilin 1 compared with that in control HL‑60 cells. These results suggest that the anticancer function of DADS on HL‑60 leukemia cells is regulated by the Rac1‑ROCK1‑LIMK1‑cofilin 1 pathway, indicating that DADS could be a promising anti‑leukemia therapeutic compound.

Indexed as

Allyl CompoundsAntineoplastic AgentsCell DifferentiationCell MovementCofilin 1DisulfidesDown-RegulationGene Expression Regulation, NeoplasticHL-60 CellsHumansLeukemiaLim KinasesPhosphorylationrac1 GTP-Binding Proteinrho-Associated KinasesSignal TransductionAllyl CompoundsAntineoplastic AgentsCFL1 protein, humanCofilin 1diallyl disulfideDisulfidesLIMK1 protein, humanLim Kinasesrac1 GTP-Binding ProteinRAC1 protein, humanrho-Associated KinasesROCK1 protein, humancofilin 1diallyl disulfidedifferentiationleukemiaproliferation

Identifiers

PMID32124958
PMCPMC7010219
OpenAlexW3002029527

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.