Evidence map›Paper›PMID 36266462›Full record

ArticleScientific reports2022

BDNF/TRKB axis provokes EMT progression to induce cell aggressiveness via crosstalk with cancer-associated fibroblasts in human parotid gland cancer.

Kazumasa Moriwaki, Masaki Wada, Hiroko Kuwabara, Yusuke Ayani, Tetsuya Terada, Masaaki Higashino, Ryo Kawata, Michio Asahi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. 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
1.3field-weighted citation impact, top 22% 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, 16 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

8 authors at 1 institution in 1 country.

Kazumasa Moriwaki *Department of Pharmacology, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan. kazumasa.moriwaki@ompu.ac.jp.
Masaki Wada *Department of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Hiroko KuwabaraDepartment of Pathology, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Yusuke AyaniDepartment of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Tetsuya TeradaDepartment of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Masaaki HigashinoDepartment of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Ryo KawataDepartment of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Michio AsahiDepartment of Pharmacology, Faculty of Medicine, Osaka Medical and Pharmaceutical University, 2-7, Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan. masahi@ompu.ac.jp.
Osaka University of Pharmaceutical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parotid gland cancer (PGC) is a rare malignancy and its molecular characteristics remain poorly understood, which has precluded the development of effective drug therapies. Given the poor prognosis of many human cancers in which tropomyosin receptor kinase B (TRKB) is highly expressed, we investigated the involvement of brain-derived neurotrophic factor (BDNF)/TRKB pathway in PGC cells using clinical specimens and observed upregulation of TRKB and BDNF. In primary culture systems of patient-derived PGC cells and cancer-associated fibroblasts (CAFs), PGC cells co-cultured with CAFs exhibited significant upregulation of BDNF and epithelial-mesenchymal transition (EMT). Similar results were observed in PGC cells treated with conditioned medium from co-cultures of PGC cells with CAFs. Administration of TRK inhibitors suppressed BDNF-induced cell migration in PGC cells. Immunohistochemical and clinicopathological analyses of tumors from patients with PGC revealed that BDNF and TRKB were highly expressed in both tumor cells and stromal cells such as CAFs, and TRKB expression levels in PGC cells were significantly correlated with aggressive features, including vascular invasion, nodal metastasis, and poor prognosis. Collectively, these data suggest that the BDNF/TRKB pathway regulates PGC cell aggressiveness via crosstalk with CAFs and is a potential therapeutic target for PGC harboring invasive and metastatic features.

Indexed as

Brain-Derived Neurotrophic FactorCancer-Associated FibroblastsReceptor, trkBSalivary Gland NeoplasmsCell Line, TumorCulture Media, ConditionedEpithelial-Mesenchymal TransitionHumansParotid GlandBrain-Derived Neurotrophic FactorCulture Media, ConditionedReceptor, trkB

Identifiers

PMID36266462
PMCPMC9584965
OpenAlexW4306879840

What OpenQuestion holds

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LicenceCC BY
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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.