Evidence map›Paper›PMID 32736413›Full record

ArticleCancer science2020

HTR3A is correlated with unfavorable histology and promotes proliferation through ERK phosphorylation in lung adenocarcinoma.

Mitsuyo Tone, Shinichiro Tahara, Satoshi Nojima, Daisuke Motooka, Daisuke Okuzaki, Eiichi Morii

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  6. Cancer and neurotransmitter receptors.Chinese medical journal · 2025
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  11. Selection of potential targets for stratifying congenital pulmonary airway malformation patients with molecular imaging: is MUC1 the one?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  12. Article
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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

6 authors at 1 institution in 1 country.

Mitsuyo ToneDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Shinichiro TaharaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0001-6134-3275
Satoshi NojimaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Daisuke MotookaSingle Cell Genomics, Human Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Daisuke OkuzakiSingle Cell Genomics, Human Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
The University of Osaka · JP

Funding

JSPS KAKENHI JP17K19555JSPS KAKENHI JP18K15078JSPS KAKENHI JP19H03452JSPS KAKENHI JP20K16171
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer death around the world. Adenocarcinoma is the most common histological type and has various histologic subtypes: lepidic, acinar, papillary, solid, and invasive mucinous adenocarcinoma. Histologic subtypes are related to invasiveness of tumors; eg, lepidic subtype is less invasive than acinar/papillary subtype. HTR3A is the main subunit of 5-hydroxytryptamine 3 (5-HT3) receptors, which are the only ligand-gated ion channels in seven families of 5-HT receptors. Although 5-HT3 receptor is expressed mainly throughout the central and peripheral nervous systems, some papers report the effect of 5-HT3 receptors on tumor cells, including lung cancer. However, whether HTR3A correlates with histopathological findings such as the histologic subtypes or the distribution in an individual sample remains unclear. Immunohistochemically, we revealed that the higher expression level of HTR3A was detected in acinar, papillary, and solid adenocarcinoma than in adenocarcinoma in situ and lepidic adenocarcinoma; the former was a more aggressive subtype than the latter. We also showed the relationship between HTR3A expression and Ki-67 positivity, widely used as a proliferation marker. Moreover, we generated HTR3A-knockdown lung adenocarcinoma cells and showed that the HTR3A knockdown attenuated proliferation by ERK phosphorylation. Our results indicated that HTR3A expression was related to proliferation in lung adenocarcinoma, by means of both in vitro and immunohistochemical assays on clinical samples. We showed the therapeutic potential of a 5-HT3 receptor antagonist, tropisetron, for the treatment of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungAgedCell ProliferationErbB ReceptorsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKi-67 AntigenMaleMiddle AgedMitogen-Activated Protein Kinase 3PhosphorylationPrognosisReceptors, Serotonin, 5-HT3Serotonin 5-HT3 Receptor AntagonistsEGFR protein, humanErbB ReceptorsHTR3A protein, humanKi-67 AntigenMitogen-Activated Protein Kinase 3Receptors, Serotonin, 5-HT3Serotonin 5-HT3 Receptor AntagonistsTropisetronERK phosphorylationHTR3Aimmunohistochemistrylung adenocarcinomaproliferation

Identifiers

PMID32736413
PMCPMC7540989
OpenAlexW3046395952

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.