Evidence map›Paper›PMID 27576314›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Induction of the mesenchymal to epithelial transition by demethylation-activated microRNA-125b is involved in the anti-migration/invasion effects of arsenic trioxide on human chondrosarcoma.

Xing Bao, Tingting Ren, Yi Huang, Shidong Wang, Fan Zhang, Kuisheng Liu, Bingxin Zheng, Wei Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  3. Arsenic in medicine: past, present and future.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
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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

8 authors at 3 institutions in 1 country.

Xing BaoMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Tingting RenMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Yi HuangMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Shidong WangMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Fan ZhangMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Kuisheng LiuMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Bingxin ZhengMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Wei GuoMusculoskeletal Tumor Center, Peking University People's Hospital, No.11 Xizhimen South Street, Beijing, 100044, People's Republic of China. bonetumor@163.com.
Peking University · CNBeijing Chest Hospital · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn addition to treating acute promyelocytic leukemia, arsenic trioxide (ATO) suppresses other solid tumors, including chondrosarcoma. However, the effects of ATO on metastasis in chondrosarcoma cells, and the underlying molecular mechanisms remain unclear.

methodsThe effects of ATO on the migratory and invasive capacities of chondrosarcoma cells were investigated by Wound healing, Transwell and EMT assays. The expression of miR-125b in human chondrosarcoma tissues and cell lines was detected by real-time PCR analysis. Bisulfite sequencing analysis (BSP) was used to detect the effects of ATO on the expression of miR-125b. The gain-of-function and loss-of-function experiments were performed on chondrosarcoma cell lines to investigate the effects of miR-125b on chondrosarcoma invasion, and to determine whether signal transducer and activator of transcription 3(Stat3) mediates these effects. Dual-luciferase reporter assay was used to identify whether Stat3 is a direct target of miR-125b.

resultsMiR-125b was significantly downregulated in human metastatic chondrosarcoma tissues and cell lines but not in non-metastatic chondrosarcoma tissues. ATO up-regulates the expression of miR-125b by the demethylation of DNA. ATO induces MET and attenuates the invasive capacities of chondrosarcoma cells through miR-125b. Stat3 was verified as a direct target of miR-125b, which is involved in ATO regulating EMT-associated traits.

conclusionsThese findings, for the first time, provides evidence that the miR-125b-mediated inhibition of Stat3 is involved in the ATO-induced attenuation of metastasis in chondrosarcoma cells.

Indexed as

3' Untranslated RegionsAnimalsAntineoplastic AgentsArsenicalsArsenic TrioxideBone NeoplasmsCell Line, TumorCell MovementChondrosarcomaDNA DemethylationDown-RegulationEpigenesis, GeneticEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumans3' Untranslated RegionsAntineoplastic AgentsArsenicalsArsenic TrioxideMicroRNAsMIRN125 microRNA, humanOxidesSTAT3 protein, humanSTAT3 Transcription FactorArsenic trioxide (ATO)ChondrosarcomaMetastatsisMicroRNA-125bSignal transducer and activator of transcription3(Stat3)

Identifiers

PMID27576314
PMCPMC5006509
OpenAlexW2510758809

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.