Evidence map›Paper›PMID 33039895›Full record

ArticleNeoplasia (New York, N.Y.)2020

Breast cancer cell debris diminishes therapeutic efficacy through heme oxygenase-1-mediated inactivation of M1-like tumor-associated macrophages.

Seung Hyeon Kim, Soma Saeidi, Xiancai Zhong, Shin-Young Gwak, Ishrat Aklima Muna, Sin-Aye Park, Seong Hoon Kim, Hye-Kyung Na, Yeonsoo Joe, Hun Taeg Chung and 3 more

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

Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Eicosanoid regulation of debris-stimulated metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Debris-stimulated tumor growth: a Pandora's box?Cancer metastasis reviews · 2021
    Review
  16. Article
  17. Heme oxygenase 1: a novel oncogene in multiple gynecological cancers.International journal of biological sciences · 2021
    Review
  18. Article
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 4 institutions in 3 countries.

Seung Hyeon KimCancer Research Institute, Seoul National University, Seoul 03087, South Korea; Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea.
Soma SaeidiTumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science, Seoul National University, Seoul 08826, South Korea.
Xiancai ZhongTumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea.
Shin-Young GwakTumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science, Seoul National University, Seoul 08826, South Korea.
Ishrat Aklima MunaTumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea.
Sin-Aye ParkDepartment of Biomedical Laboratory Science, College of Medical Sciences, Soonchunhyang University, Asan 31538, South Korea.
Seong Hoon KimTumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea.
Hye-Kyung NaDepartment of Food Science and Biotechnology, College of Knowledge-based Services Engineering, Sungshin Women's University, Seoul 01133, South Korea.
Yeonsoo JoeDepartment of Biological Sciences, University of Ulsan, Ulsan 44610, South Korea.
Hun Taeg ChungDepartment of Biological Sciences, University of Ulsan, Ulsan 44610, South Korea.
Kyoung-Eun KimDepartment of Surgery, Seoul National University College of Medicine, Seoul 03087, South Korea.
Wonshik HanDepartment of Surgery, Seoul National University College of Medicine, Seoul 03087, South Korea.
Young-Joon SurhCancer Research Institute, Seoul National University, Seoul 03087, South Korea; Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science, Seoul National University, Seoul 08826, South Korea. Electronic address: surh@snu.ac.kr.
Seoul National University · KRUniversity of Ulsan · KRSoonchunhyang University · KRSungshin Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is commonly used as a major therapeutic option for breast cancer treatment, but its efficacy is often diminished by disruption of patient's anti-tumor immunity. Chemotherapy-generated tumor cell debris could hijack accumulated tumor-associated macrophages (TAMs), provoking tumor recurrence. Therefore, reprogramming TAMs to acquire an immunocompetent phenotype is a promising strategy to potentiate therapeutic efficacy. In this study, we analyzed the proportion of immune cells in the breast cancer patients who received chemotherapy. To validate our findings in vivo, we used a syngeneic murine breast cancer (4T1) model. Chemotherapy generates an immunosuppressive tumor microenvironment in breast cancer. Here, we show that phagocytic engulfment of tumor cell debris by TAMs reduces chemotherapeutic efficacy in a 4T1 breast cancer model. Specifically, the engulfment of tumor cell debris by macrophages reduced M1-like polarization through heme oxygenase-1 (HO-1) upregulation. Conversely, genetic or pharmacologic inhibition of HO-1 in TAMs restored the M1-like polarization. Our results demonstrate that tumor cell debris-induced HO-1 expression in macrophages regulates their polarization. Inhibition of HO-1 overexpression in TAMs may provoke a robust anti-tumor immune response, thereby potentiating the efficacy of chemotherapy.

Indexed as

AnimalsBiomarkers, TumorBreast NeoplasmsCell Line, TumorDisease Models, AnimalDisease SusceptibilityFemaleGene Expression Regulation, NeoplasticHeme Oxygenase-1HumansImmunophenotypingMacrophage ActivationMiceModels, BiologicalPhagocytosisTumor-Associated MacrophagesBiomarkers, TumorHeme Oxygenase-1Breast cancerChemotherapyHeme oxygenase-1PhagocytosisTumor-associated macrophagesTumor cell debris

Identifiers

PMID33039895
PMCPMC7581991
OpenAlexW3092637742

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.