Evidence map›Paper›PMID 28054649›Full record

ArticleScientific reports2017

Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to doxorubicin via Src-Stat3 inactivation in osteosarcoma.

Toshinori Ando, Yasusei Kudo, Shinji Iizuka, Takaaki Tsunematsu, Hanako Umehara, Madhu Shrestha, Toshihiro Matsuo, Tadahiko Kubo, Shouji Shimose, Koji Arihiro and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

13 authors at 5 institutions in 1 country.

Toshinori AndoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yasusei KudoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shinji IizukaDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takaaki TsunematsuDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hanako UmeharaDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Madhu ShresthaDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Toshihiro MatsuoDepartment of Orthopedic Surgery, Aichi Medical University, Nagakute, Aichi, Japan.
Tadahiko KuboDepartment of Orthopaedic Surgery, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shouji ShimoseDivision of Orthopaedic Surgery, National Hospital Organization Kure Medical Center, Kure, Japan.
Koji ArihiroAnatomical Pathology, Hiroshima University Hospital, Hiroshima, Japan.
Ikuko OgawaCenter of Oral Clinical Examination, Hiroshima University Hospital, Hiroshima, Japan.
Mitsuo OchiDepartment of Orthopaedic Surgery, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takashi TakataDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPHiroshima University Hospital · JPTokushima University · JPAichi Medical University · JPNational Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ameloblastin (AMBN), the most abundant non-amelogenin enamel matrix protein, plays a role in ameloblast differentiation. Previously, we found that AMBN promoted osteogenic differentiation via the interaction between CD63 and integrin β1, leading to the inactivation of Src; however, how AMBN affects the malignant behavior of osteosarcoma is still unclear. Osteosarcoma affects the bone and is associated with poor prognosis because of the high rate of pulmonary metastases and drug resistance. Here we demonstrated that stable overexpression of AMBN induced apoptosis and suppressed colony formation and cell migration via the inactivation of Src-Stat3 pathway in human osteosarcoma cells. Moreover, AMBN induced chemosensitivity to doxorubicin. Thus, AMBN induced a tumor suppressive phenotype and chemosensitivity to doxorubicin via the AMBN-Src-Stat3 axis in osteosarcoma. Indeed, immunohistochemical expression of AMBN was significantly correlated with better outcome of osteosarcoma patients. Our findings suggest that AMBN can be a new prognostic marker and therapeutic target for osteosarcoma combined with conventional doxorubicin treatment.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalDental Enamel ProteinsDisease Models, AnimalDoxorubicinHumansImmunohistochemistryMice, NudeModels, BiologicalNeoplasm TransplantationOncogene Protein pp60(v-src)AMBN protein, humanAntibiotics, AntineoplasticDental Enamel ProteinsDoxorubicinOncogene Protein pp60(v-src)STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID28054649
PMCPMC5214574
OpenAlexW2567729469

What OpenQuestion holds

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Registered trials

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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.