Evidence map›Paper›PMID 26743690›Full record

ArticleScientific reports2016

Dihydroartemisinin prevents breast cancer-induced osteolysis via inhibiting both breast caner cells and osteoclasts.

Ming-Xuan Feng, Jian-Xin Hong, Qiang Wang, Yong-Yong Fan, Chi-Ting Yuan, Xin-Huan Lei, Min Zhu, An Qin, Hai-Xiao Chen, Dun Hong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.5field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  9. Pharmaceutics · 2023
    Article
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  16. Article
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  18. Article
  19. Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Ming-Xuan FengOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Jian-Xin HongOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Qiang WangOrthopaedic Department, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310016, China.
Yong-Yong FanOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Chi-Ting YuanOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Xin-Huan LeiOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Min ZhuOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
An QinOrthopaedic Department, Shanghai Key Laboratory of Orthopaedic Implant, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011,China.
Hai-Xiao ChenOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Dun HongOrthopaedic Department, Taizhou Hospital, Wenzhou Medical University, Linhai, 317000, China.
Wenzhou Medical University · CNShanghai Ninth People's Hospital · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone is the most common site of distant relapse in breast cancer, leading to severe complications which dramatically affect the patients' quality of life. It is believed that the crosstalk between metastatic breast cancer cells and osteoclasts is critical for breast cancer-induced osteolysis. In this study, the effects of dihydroartemisinin (DHA) on osteoclast formation, bone resorption, osteoblast differentiation and mineralization were initially assessed in vitro, followed by further investigation in a titanium-particle-induced osteolysis model in vivo. Based on the proved inhibitory effect of DHA on osteolysis, DHA was further applied to MDA-MB-231 breast cancer-induced mouse osteolysis model, with the underlying molecular mechanisms further investigated. Here, we verified for the first time that DHA suppressed osteoclast differentiation, F-actin ring formation and bone resorption through suppressing AKT/SRC pathways, leading to the preventive effect of DHA on titanium-particle-induced osteolysis without affecting osteoblast function. More importantly, we demonstrated that DHA inhibited breast tumor-induced osteolysis through inhibiting the proliferation, migration and invasion of MDA-MB-231 cells via modulating AKT signaling pathway. In conclusion, DHA effectively inhibited osteoclastogenesis and prevented breast cancer-induced osteolysis.

Indexed as

Gene Expression Regulation, NeoplasticActinsAnimalsArtemisininsBone DensityBreast NeoplasmsCell DifferentiationCell Line, TumorCell MovementFemaleHumansMiceMice, Inbred C57BLOsteoblastsOsteoclastsOsteolysisActinsArtemisininsartenimolProto-Oncogene Proteins c-aktsrc-Family KinasesTitanium

Identifiers

PMID26743690
PMCPMC4705478
OpenAlexW2226301192

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.