Evidence map›Paper›PMID 23895248›Full record

ArticleCell communication and signaling : CCS2013

Mitochondrial translocation of cofilin is required for allyl isothiocyanate-mediated cell death via ROCK1/PTEN/PI3K signaling pathway.

Guo-bing Li, Qi Cheng, Lei Liu, Ting Zhou, Chang-yu Shan, Xiao-ye Hu, Jing Zhou, E-hu Liu, Ping Li, Ning Gao

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Cofilin: A Promising Protein Implicated in Cancer Metastasis and Apoptosis.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease.Frontiers in cell and developmental biology · 2020
    Review
  20. 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

10 authors at 2 institutions in 1 country.

Guo-bing LiDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing 400038, China.
Qi Cheng
Lei Liu
Ting Zhou
Chang-yu Shan
Xiao-ye Hu
Jing Zhou
E-hu Liu
Ping Li
Ning Gao
Army Medical University · CNChina Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCofilin is a member of the actin depolymerizing factor (ADF)/cofilin family, which regulates actin dynamics. Increasing evidence suggests that mitochondrial translocation of cofilin appears necessary for the regulation of apoptosis.

resultsWe report that allyl isothiocyanate (AITC) potently induces mitochondria injury and apoptosis. These events were accompanied by a loss of polymerized filamentous actin (F-actin) and increase in unpolymerized globular actin (G-actin). AITC also induces dephosphorylation of cofilin through activation of PP1 and PP2A. Only dephosphorylated cofilin binds to G-actin and translocates to mitochondria during AITC-mediated apoptosis. Mechanistic study revealed that interruption of ROCK1/PTEN/PI3K signaling pathway plays a critical role in AITC-mediated dephosphorylation and mitochondrial translocation of cofilin and apoptosis. Our in vivo study also showed that AITC-mediated inhibition of tumor growth of mouse leukemia xenograft model is in association with dephosphorylation of cofilin.

conclusionsThese findings support a model in which induction of apoptosis by AITC stems primarily from activation of ROCK1 and PTEN, and inactivation of PI3K, leading in turn to activation of PP1 and PP2A, resulting in dephosphorylation of cofilin, which binds to G-actin and translocates to mitochondria, culminating in the dysfunction of mitochondria, release of cytochrome c and apoptosis.

Indexed as

ActinsAnimalsAntineoplastic AgentsApoptosisCells, CulturedCofilin 1HL-60 CellsHumansIsothiocyanatesJurkat CellsLeukemiaMiceMice, NudeMitochondriaPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsActinsallyl isothiocyanateAntineoplastic AgentsCFL1 protein, humanCofilin 1IsothiocyanatesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPTEN PhosphohydrolasePTEN protein, humanrho-Associated KinasesROCK1 protein, human

Identifiers

PMID23895248
PMCPMC3734051
OpenAlexW2158366150

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.