Evidence map›Paper›PMID 32976685›Full record

ArticleCancer medicine2020

Asperolide A prevents bone metastatic breast cancer via the PI3K/AKT/mTOR/c-Fos/NFATc1 signaling pathway.

Wenli Jiang, Youlutuziayi Rixiati, Hao Huang, YiJun Shi, Caiguo Huang, Binghua Jiao

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. Peritoneal cavity-derived GATA6Journal of advanced research · 2026
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  12. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  13. Review
  14. Anti-lung Cancer Marine Compounds: A Review.Therapeutic innovation & regulatory science · 2022
    Review
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  16. Article
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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 1 country.

Wenli JiangDepartment of Biochemistry and Molecular Biology, College of Basic Medical, Navy Medical University, Shanghai, China.
Youlutuziayi RixiatiDepartment of Pathology, Soochow University Medical School, Suzhou, China.
Hao HuangDepartment of Orthopaedics, Shaoxing People's Hospital, Shaoxing, China.
YiJun ShiDepartment of Biochemistry and Molecular Biology, College of Basic Medical, Navy Medical University, Shanghai, China.
Caiguo HuangDepartment of Biochemistry and Molecular Biology, College of Basic Medical, Navy Medical University, Shanghai, China.
Binghua JiaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical, Navy Medical University, Shanghai, China.ORCID 0000-0002-9606-2665
Shanghai Medical College of Fudan University · CNShaoxing People's Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer is the leading cause of death among women with malignant tumors worldwide. Bone metastasis is the main factor affecting the prognosis of breast cancer. Therefore, both antitumor and anti-breast-cancer-induced osteolysis agents are urgently needed.

methodsWe examined the effect of Asperolide A (AA), a marine-derived agent, on osteolysis and RANKL-induced phosphoinositide 3-kinase (PI3K)/AKT/mTOR/c-FOS/nuclear factor-activated T cell 1 (NFATc1) pathway activation, F-actin ring formation, and reactive oxygen species (ROS) generation in vitro. We evaluated AA effect on breast cancer MDA-MB-231 and MDA-MB-436 cells in vitro through CCK8 assay, wound healing assay, transwell assay, Annexin V-FITC/PI staining for cell apoptosis, and cell cycle assay. Furthermore, we assessed the effect of AA in vivo using a breast cancer-induced bone osteolysis nude mouse model, followed by micro-computed tomography, tartrate-resistant acid phosphatase staining, and hematoxylin and eosin staining.

resultsAsperolide A inhibited osteoclast formation and differentiation, bone resorption, F-actin belt formation, ROS activity, and osteoclast-specific gene and protein expressions and prevented PI3K/AKT/mTOR/c-FOS/NFATc1 signaling activation in a dose-dependent manner in vitro. AA also inhibited breast cancer growth and breast cancer-induced bone osteolysis by reducing osteoclast formation and function and inactivated PI3K/AKT/mTOR signaling in vivo.

conclusionsOur study demonstrated that AA suppressed bone metastatic breast cancer. These findings indicate AA as a potential, novel curative drug candidate for patients with bone metastatic breast cancer.

Indexed as

ActinsAnimalsApoptosisBone NeoplasmsBreast NeoplasmsCell Cycle CheckpointsCell DifferentiationCell Line, TumorCell MovementCell ProliferationDiterpenesFemaleGene ExpressionHumansMacrophagesMiceActinsasperolide ADiterpenesMTOR protein, humanmTOR protein, mouseNFATC1 protein, humanNfatc1 protein, mouseNFATC Transcription FactorsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fosRANK LigandReactive Oxygen SpeciesTOR Serine-Threonine KinasesAsperolide Abone metastasesbreast cancermTORosteoclast

Identifiers

PMID32976685
PMCPMC7643645
OpenAlexW3088255781

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.