Evidence map›Paper›PMID 24691407›Full record

ArticlePloS one2014

VASP activation via the Gα13/RhoA/PKA pathway mediates cucurbitacin-B-induced actin aggregation and cofilin-actin rod formation.

Yan-Ting Zhang, Li-Hui Xu, Qun Lu, Kun-Peng Liu, Pei-Yan Liu, Fang Ji, Xiao-Ming Liu, Dong-Yun Ouyang, Xian-Hui He

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Recent Advances in the Application of Cucurbitacin B as an Anticancer Agent.International journal of molecular sciences · 2025
    Review
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  17. Identifying microRNA-mRNA regulatory network in gemcitabine-resistant cells derived from human pancreatic cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  18. 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

9 authors at 4 institutions in 2 countries.

Yan-Ting ZhangDepartment of Immunobiology, Jinan University, Guangzhou, China.
Li-Hui XuDepartment of Cell Biology, Jinan University, Guangzhou, China.
Qun LuDepartment of Anatomy and Cell Biology, East Carolina University Brody School of Medicine, Greenville, North Carolina, United States of America.
Kun-Peng LiuDepartment of Immunobiology, Jinan University, Guangzhou, China.
Pei-Yan LiuDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Fang JiGuangdong Entomological Institute, Guangzhou, China.
Xiao-Ming LiuSouthern China Primate Research Center, Guangzhou, China.
Dong-Yun OuyangDepartment of Immunobiology, Jinan University, Guangzhou, China.
Xian-Hui HeDepartment of Immunobiology, Jinan University, Guangzhou, China.
Jinan University · CNEast Carolina University · USFirst Affiliated Hospital of Jinan University · CNYunnan Yingmao Biotechnology (China) · CN

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
NCI NIH HHS P30 CA016086
6 · The paper itself

Abstract

Cucurbitacin B (CuB), a potent antineoplastic agent of cucurbitacin triterpenoids, induces rapid disruption of actin cytoskeleton and aberrant cell cycle inhibiting carcinogenesis. However, the underlying molecular mechanism of such anticancer effects remains incompletely understood. In this study, we showed that CuB treatment rapidly induced vasodilator-stimulated phosphoprotein (VASP) phosphorylation (i.e. activation) at the Ser157 residue and generated VASP clumps which were co-localized with amorphous actin aggregates prior to the formation of highly-ordered cofilin-actin rods in melanoma cells. Knockdown of VASP or inhibition of VASP activation using PKA-specific inhibitor H89 suppressed CuB-induced VASP activation, actin aggregation and cofilin-actin rod formation. The VASP activation was mediated by cAMP-independent PKA activation as CuB decreased the levels of cAMP while MDL12330A, an inhibitor of adenylyl cyclase, had weak effect on VASP activation. Knockdown of either Gα13 or RhoA not only suppressed VASP activation, but also ameliorated CuB-induced actin aggregation and abrogated cofilin-actin rod formation. Collectively, our studies highlighted that the CuB-induced actin aggregation and cofilin-actin rod formation was mediated via the Gα13/RhoA/PKA/VASP pathway.

Indexed as

Actin CytoskeletonActin Depolymerizing FactorsAnimalsCarcinogenesisCell Adhesion MoleculesCell CycleCell ProliferationCyclic AMP-Dependent Protein KinasesHumansMelanoma, ExperimentalMiceMicrofilament ProteinsPhosphoproteinsProtein AggregatesrhoA GTP-Binding Proteinrho GTP-Binding ProteinsActin Depolymerizing FactorsCell Adhesion Moleculescucurbitacin BCyclic AMP-Dependent Protein KinasesMicrofilament ProteinsPhosphoproteinsProtein AggregatesrhoA GTP-Binding ProteinRhoA protein, mouserho GTP-Binding ProteinsTriterpenesVasodilator-Stimulated Phosphoprotein

Identifiers

PMID24691407
PMCPMC3972149
OpenAlexW2077115046

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.