Evidence map›Paper›PMID 36477408›Full record

ArticleCell death & disease2022

Laminins in tumor-derived exosomes upregulated by ETS1 reprogram omental macrophages to promote omental metastasis of ovarian cancer.

Haiyang Li, Cheng Zeng, Chang Shu, Yuanyuan Cao, Wengui Shao, Mengjie Zhang, Hongyong Cao, Shuli Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. Article
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  7. Article
  8. Article
  9. New insights into extracellular vesicles in metastatic cancer: From mechanisms to diagnostics and targeted therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Effect of Extracellular Vesicles Derived From Tumor Cells on Immune Evasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025
    Review
  19. 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

8 authors at 2 institutions in 1 country.

Haiyang LiDepartment of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Cheng ZengGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Chang ShuGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Yuanyuan CaoGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Wengui ShaoGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Mengjie ZhangGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Hongyong CaoDepartment of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. caohongy6167@163.com.ORCID 0000-0003-1188-991X
Shuli ZhaoGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. shulizhao79@njmu.edu.cn.ORCID 0000-0002-3610-2418
China Pharmaceutical University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-derived exosomes participate in omental metastatic colonization of ovarian cancer by inducing an adaptive response in the tumor microenvironment. However, cell-cell communication via exosomes between primary tumor cells and the microenvironment of distant omentum and the mechanism of pre-metastatic niche formation are poorly understood. Here, we demonstrated that ETS1-overexpressing ovarian cancer cells secreted larger exosomes with higher laminin levels. In addition, ovarian cancer exosomes could be taken up by omental macrophages through integrin and laminin interaction. Compared with control exosomes, exosomes derived from ETS1-overexpressing ovarian cancer cells (LV-ETS1 Exos) stimulated the polarization of more macrophages toward the M2 phenotype (CD163 marker), as well as the production of more CXCL5 and CCL2 in macrophages, via integrin αvβ5/AKT/Sp1 signaling. In vivo experiments showed that LV-ETS1 Exos promoted omental metastasis of ovarian cancer by mediating the tumor-promoting effect of macrophages, which could be neutralized by integrin ανβ5 inhibitor cilengitide. These results indicated that ETS1 could drive ovarian cancer cells to release exosomes with higher laminin levels, thereby accelerating the exosome-mediated pro-metastatic effects of omental macrophages via the integrin αvβ5/AKT/Sp1 signaling pathway, and the integrin ανβ5 inhibitor cilengitide could inhibit omental metastasis of ovarian cancer driven by tumor-derived exosomes.

Indexed as

LamininOvarian NeoplasmsFemaleHumansIntegrinsProto-Oncogene Protein c-ets-1Tumor MicroenvironmentETS1 protein, humanIntegrinsLamininProto-Oncogene Protein c-ets-1

Identifiers

PMID36477408
PMCPMC9729302
OpenAlexW4311572503

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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.