Evidence map›Paper›PMID 31878245›Full record

ArticleCancers2019

Ovatodiolide Suppresses Oral Cancer Malignancy by Down-Regulating Exosomal Mir-21/STAT3/β-Catenin Cargo and Preventing Oncogenic Transformation of Normal Gingival Fibroblasts.

Jia-Hong Chen, Alexander T H Wu, Oluwaseun Adebayo Bamodu, Vijesh Kumar Yadav, Tsu-Yi Chao, Yew-Min Tzeng, Debabrata Mukhopadhyay, Michael Hsiao, Jih-Chin Lee

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

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  11. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
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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

9 authors at 6 institutions in 2 countries.

Jia-Hong ChenGraduate and Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Alexander T H WuThe PhD Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Oluwaseun Adebayo BamoduDepartment of Hematology and Oncology, Cancer Center, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.
Vijesh Kumar YadavThe Program for Translational Medicine, Graduate Institute of Biomedical Informatics, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Tsu-Yi ChaoDepartment of Hematology and Oncology, Cancer Center, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.
Yew-Min TzengCenter for General Education, National Taitung University, Taitung 95092, Taiwan.
Debabrata MukhopadhyayDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei City 11529, Taiwan.
Jih-Chin LeeDepartment of Otolaryngology, Head and Neck Surgery Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Taipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TWTri-Service General Hospital · TWKaohsiung Medical University · TWMayo Clinic · USNational Taitung University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 108-2314-B-016 -039, MOST 107-2314-B-016 -028Tri-Service General Hospital TSGH-2-C108-108-2314-B-016-039Tri-Service General Hospital TSGH-C107-030
6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) is among the most commonly diagnosed malignancies in the world. Patients with OSCC often develop treatment resistance, resulting in a poor prognosis. Mounting evidence indicates that interactions between cancerous cells and other components of the tumor microenvironment (TME) determine their response to treatment. Herein, we examined the role of cancer stem cell-derived extracellular vesicles (CSC_EVs) generated from CAL27 and SCC-15 OSCC cells in the development of cisplatin (CDDP) resistance. We demonstrated that CSC_EVs enhance CDDP resistance, clonogenicity, and the tumorsphere formation potential of OSCC cells. Our bioinformatics analyses revealed that OSCC_EVs are enriched with microRNA (miR)-21-5p and are associated with increased metastasis, stemness, chemoresistance, and poor survival in patients with OSCC. Mechanistically, enhanced activity of CSC_EVs was positively correlated with upregulated β-catenin, phosphatidylinositol-3 kinase (PI3K), signal transducer and activator of transcription 3 (STAT3), mammalian target of rapamycin (mTOR), and transforming growth factor (TGF)-β1 messenger (m)RNA and protein expression levels. CSC_EVs also conferred a cancer-associated fibroblast (CAF) phenotype on normal gingival fibroblasts (NGFs), with the resultant CAFs enhancing the oncogenicity of OSCC cells. Interestingly, treatment with ovatodiolide (OV), the bioactive component of

Indexed as

cancer-associated fibroblastsextracellular vesiclesmiR-21-5p/STAT3/β-catenin signalingoral squamous cell carcinomaovatodiolidetumor microenvironment

Identifiers

PMID31878245
PMCPMC7017298
OpenAlexW2997862810

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.