Evidence map›Paper›PMID 30872795›Full record

ArticleOncogene2019

Hypoxia-induced tumor exosomes promote M2-like macrophage polarization of infiltrating myeloid cells and microRNA-mediated metabolic shift.

Jung Eun Park, Bamaprasad Dutta, Shun Wilford Tse, Nikhil Gupta, Chee Fan Tan, Jee Keem Low, Kheng Wei Yeoh, Oi Lian Kon, James P Tam, Siu Kwan Sze

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed
–field-weighted citation impact
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

218 citing papers in PubMed.

  1. Towards liquid biopsy-based analysis of antitumour immunity.Nature reviews. Clinical oncology · 2026
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  12. Article
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  15. Current trends in exosomes as therapeutic drug delivery systems.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

158 more citing papers are in PubMed but not listed here.

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

10 authors.

Jung Eun ParkSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore. jepark@ntu.edu.sg.
Bamaprasad DuttaSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.
Shun Wilford TseSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.
Nikhil GuptaSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.
Chee Fan TanSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.
Jee Keem LowDepartment of Surgery, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore, 308433, Singapore.
Kheng Wei YeohNational Cancer Centre Singapore, Department of Radiation Oncology, 11 Hospital Drive, Singapore, 169610, Singapore.
Oi Lian KonNational Cancer Centre Singapore, Division of Medical Sciences, 11 Hospital Drive, Singapore, 169610, Singapore.
James P TamSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.
Siu Kwan SzeSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore. sksze@ntu.edu.sg.ORCID http://orcid.org/0000-0002-5652-1687

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Developing tumors rapidly outgrow their oxygen supply and are subject to hypoxia, which stimulates hypersecretion of tumor-derived exosomes that promote angiogenesis, metastasis, and immunosuppression, but the molecular mediators of these pathological effects remain poorly defined. Using quantitative proteomics, we identified that exosomes produced by hypoxic tumor cells are highly enriched in immunomodulatory proteins and chemokines including CSF-1, CCL2, FTH, FTL, and TGFβ. Modeling exosome effects on tumor-infiltrating immune cells, we observed a potent ability of these hypoxia-induced vesicles to influence macrophage recruitment and promote M2-like polarization both in vitro and in vivo. In addition, hypoxic, but not normoxic, tumor exosomes enhanced oxidative phosphorylation in bone marrow-derived macrophages via transfer of let-7a miRNA, resulting in suppression of the insulin-Akt-mTOR signaling pathway. Together, these data demonstrate that hypoxia promotes tumor secretion of biomolecule-loaded exosomes that can modify the immunometabolic profile of infiltrating monocyte-macrophages to better evade host immunity and enhance tumor progression.

Indexed as

Oxidative PhosphorylationA549 CellsAnimalsCell MovementCell PolarityCells, CulturedChemotaxis, LeukocyteExosomesHumansMacrophagesMaleMetabolomeMiceMice, Inbred C57BLMicroRNAsMyeloid CellsMicroRNAs

Identifiers

What OpenQuestion holds

Textmetadata
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.