Evidence map›Paper›PMID 35000146›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2022

MiR-192-5p-Modified Tumor-Associated Macrophages-Derived Exosome Suppressed Endometrial Cancer Progression Through Targeting IRAK1/NF-κB Signaling.

Yilin Wang, Hongsheng Ma, Yajie Li, Rina Su

Abstract read
PubMed Publisher
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  4. Transcriptional Repression of CCL2 by KInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Review
  7. Exosomal ncRNAs in reproductive cancers†.Biology of reproduction · 2025
    Review
  8. Article
  9. Review
  10. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
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  13. 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

4 authors at 2 institutions in 1 country.

Yilin WangDepartment of Obstetrics and Gynecology, Inner Mongolia People's Hospital, 20 Zhaowuda Road, Saihan District, Hohhot City, Inner Mongolia, China.
Hongsheng MaDepartment of Obstetrics and Gynecology, Inner Mongolia People's Hospital, 20 Zhaowuda Road, Saihan District, Hohhot City, Inner Mongolia, China. HongshengMa@protonmail.com.ORCID 0000-0003-2101-878X
Yajie LiHohhot Maternal and Child Health Care Hospital, 33 Baotou Street, Yuquan District, Hohhot City, Inner Mongolia, China.
Rina SuDepartment of Obstetrics and Gynecology, Inner Mongolia People's Hospital, 20 Zhaowuda Road, Saihan District, Hohhot City, Inner Mongolia, China.
Inner Mongolia People's Hospital · CNInner Mongolia Maternal and Child Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) are a major regulator in the development of endometrial cancer (EC). It was indicated that TAMs could crosstalk with cancer cells via transferring exosomes which carrying microRNAs (miRNAs). Firstly, we found that TAMs could promote the epithelial-mesenchymal transition (EMT) of EC cells and inhibit its apoptosis. Next, we further found that TAMs regulated the EMT and apoptosis of EC cells through transferring exosomes into EC cells. Then, lowly expressed miR-192-5p in TAMs-derived exosomes was proved. Moreover, our data demonstrated that upregulation of miR-192-5p in TAMs-derived exosomes could significantly promote the apoptosis of EC cells and impede its EMT. IRAK1 was proved to be a downstream target of miR-192-5p. Importantly, we indicated that miR-192-5p-overexpressed TAMs-derived exosomes regulated the EC cells apoptosis and EMT through inhibiting IRAK1/NF-κB signaling pathway. In addition, we also revealed that overexpression of miR-192-5p in TAMs-derived exosomes obviously limits the growth of tumors. Overall, in TAMs-derived exosomes, our data demonstrated that overexpression of miR-192-5p could effectively suppress the progression of EC. Our data provid a new target for EC treatment.

Indexed as

Signal TransductionTumor-Associated MacrophagesAnimalsApoptosisEndometrial NeoplasmsExosomesFemaleHumansInterleukin-1 Receptor-Associated KinasesMiceMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm TransplantationNF-kappa BPolymerase Chain ReactionInterleukin-1 Receptor-Associated KinasesIRAK1 protein, humanMicroRNAsMIRN192 microRNA, humanNF-kappa BCompeting endogenous RNAEndometrial cancerExosomesmiR-192-5pTumor-associated macrophages

Identifiers

PMID35000146
OpenAlexW4205385215

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.