Evidence map›Paper›PMID 36411518›Full record

ArticleCancer science2023

Depletion of tumor-associated macrophages inhibits lung cancer growth and enhances the antitumor effect of cisplatin.

Yo Kawaguchi, Yasuhiko Ohshio, Atsuko Watanabe, Takuya Shiratori, Keigo Okamoto, Keiko Ueda, Yoko Kataoka, Tomoaki Suzuki, Jun Hanaoka

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  12. COX-2 in lung cancer: Mechanisms, development, and targeted therapies.Chronic diseases and translational medicine · 2024
    Review
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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 1 institution in 1 country.

Yo KawaguchiDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.ORCID https://orcid.org/0000-0002-7828-4635
Yasuhiko OhshioDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Atsuko WatanabeDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Takuya ShiratoriDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Keigo OkamotoDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Keiko UedaDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Yoko KataokaDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Tomoaki SuzukiDivision of Cardiovascular Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Jun HanaokaDivision of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Otsu, Japan.
Shiga University of Medical Science · JP

Funding

YOKOYAMA Foundation YRY-2005
6 · The paper itself

Abstract

In lung cancer, tumor-associated macrophages (TAMs), especially M2-like TAMs, represent the main tumor progression components in the tumor microenvironment (TME). Therefore, M2-like TAMs may serve as a therapeutic target. The purpose of this study was to investigate the effect of M2-like TAM depletion in the TME on tumor growth and chemotherapy response in lung cancer. The levels of secreted monocyte chemoattractant protein (MCP-1) and prostaglandin E2 (PGE2) in the supernatants of lung cancer cell lines A549 and LLC were evaluated via ELISA. Cell migration assays were performed to assess the recruitment ability of macrophage cell lines THP-1 and J774-1 cells. Differentiation of macrophages was assessed via flow cytometry. Immunohistochemical staining was performed to visualize M2-like TAMs in transplanted lung cancer in mouse. We used the COX-2 inhibitor nimesulide to inhibit the secretion of MCP-1 and PGE2, which promotes macrophage migration and M2-like differentiation. Nimesulide treatment decreased the secretion of MCP-1 and PGE2 from lung cancer cells. Nimesulide treatment suppressed the migration of macrophages by blocking MCP-1. Lung cancer supernatant induced the differentiation of macrophages toward the M2-like phenotype, and nimesulide treatment inhibited M2-like differentiation by blocking MCP-1 and PGE2. In the lung cancer mouse model, treatment with nimesulide depleted M2-like TAMs in the TME and enhanced the tumor inhibitory effect of cisplatin. Our results indicated that blocking the secretion of MCP-1 and PGE2 from tumor cells depleted M2-like TAMs in the TME and the combination therapy with cisplatin considerably suppressed tumor growth in the LLC mouse model.

Indexed as

CisplatinLung NeoplasmsAnimalsCell Line, TumorDinoprostoneMiceSulfonamidesTumor-Associated MacrophagesTumor MicroenvironmentCisplatinDinoprostonenimesulideSulfonamideslung cancerM2-like tumor-associated macrophagesmonocyte chemoattractant protein-1prostaglandin E2tumor microenvironment

Identifiers

PMID36411518
PMCPMC9986097
OpenAlexW4309666029

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.