Evidence map›Paper›PMID 35108425›Full record

ArticleCancer science2022

MEK/ERK-mediated oncogenic signals promote secretion of extracellular vesicles by controlling lysosome function.

Tomoya Hikita, Ryo Uehara, Reina E Itoh, Fumie Mitani, Mamiko Miyata, Takuya Yoshida, Rui Yamaguchi, Chitose Oneyama

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Role of SNHGs in Adverse Prognostic Factors in Cervical Cancer: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Exosomal ncRNAs in reproductive cancers†.Biology of reproduction · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  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

8 authors at 3 institutions in 1 country.

Tomoya HikitaDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.
Ryo UeharaDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.
Reina E ItohDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.
Fumie MitaniDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.
Mamiko MiyataDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.
Takuya YoshidaLaboratory of Biophysical Chemistry, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
Rui YamaguchiDivision of Cancer Systems Biology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Chitose OneyamaDivision of Cancer Cell Regulation, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID https://orcid.org/0000-0002-5719-9431
Aichi Cancer Center · JPNagoya City University · JPOsaka University of Pharmaceutical Sciences · JP

Funding

Japan Science and Technology Agency 20H03456Precursory Research for Embryonic Science and Technology JP1005457
6 · The paper itself

Abstract

Cancer cells secrete large amounts of extracellular vesicles (EVs) originating from multivesicular bodies (MVBs). Mature MVBs fuse either with the plasma membrane for release as EVs, often referred as to exosomes or with lysosomes for degradation. However, the mechanisms regulating MVB fate remain unknown. Here, we investigated the regulators of MVB fate by analyzing the effects of signaling inhibitors on EV secretion from cancer cells engineered to secrete luciferase-labeled EVs. Inhibition of the oncogenic MEK/ERK pathway suppressed EV release and activated lysosome formation. MEK/ERK-mediated lysosomal inactivation impaired MVB degradation, resulting in increased EV secretion from cancer cells. Moreover, MEK/ERK inhibition prevented c-MYC expression and induced the nuclear translocation of MiT/TFE transcription factors, thereby promoting the activation of lysosome-related genes, including the gene encoding a subunit of vacuolar-type H

Indexed as

Extracellular VesiclesVacuolar Proton-Translocating ATPasesGenes, mycHumansLysosomesMitogen-Activated Protein Kinase KinasesOncogenesMitogen-Activated Protein Kinase KinasesVacuolar Proton-Translocating ATPasesc-MYCextracellular vesicleslysosomeMEK/ERKrenal cancer

Identifiers

PMID35108425
PMCPMC8990735
OpenAlexW4210419463

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.