Evidence map›Paper›PMID 40318053›Full record

ReviewInternational journal of cancer2025

Exosomes, autophagy, and cancer: A complex triad.

María Guerra-Andrés, Álvaro F Fernández, Tania Fontanil

Abstract readReview
In one paragraph

Review in International journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025
    Review
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

3 authors.

María Guerra-AndrésDepartamento de Bioquímica y Biología Molecular, Universidad de Oviedo, Oviedo, Spain.
Álvaro F FernándezDepartamento de Bioquímica y Biología Molecular, Universidad de Oviedo, Oviedo, Spain.ORCID 0000-0002-7704-4285
Tania FontanilInstituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain.ORCID 0000-0003-2261-7661

Funding

Ministerio de Ciencia, Innovación y Universidades MCIU-25-CNS2024-154954Ministerio de Ciencia, Innovación y Universidades PID2021-127534OB-I00Ministerio de Universidades MCIU-20-BG20/00030
6 · The paper itself

Abstract

Cancer remains one of the leading causes of death worldwide. Despite remarkable progress in prevention, diagnosis, and therapy, the incidence of certain types of cancer persists, urging the identification of clinically relevant biomarkers and the development of novel therapeutic strategies to improve clinical outcomes and overcome treatment resistance. Exosomes, small extracellular vesicles released by diverse types of cells, have attracted interest in biomedical research due to their potential as carriers for different treatments. Moreover, exosomes play a pivotal role in intercellular communication, modulating various cellular processes. One of those is autophagy, a pro-survival pathway that is essential for human cells. Even though autophagy is traditionally described as a catabolic route, its machinery is intricately involved in various cellular responses, including vesicle formation and secretion. In this regard, the link between autophagy and exosomes is complex, bidirectional, and highly dependent on the cellular context. Interestingly, both processes have been extensively implicated in cancer pathogenesis, highlighting their potential as therapeutic targets. This review updates our understanding of how exosomes can participate in cancer development and progression, with a specific focus on their influence on tumor growth, angiogenesis, and metastasis. Additionally, the interplay between these extracellular vesicles and autophagy is minutely reviewed and discussed, as we hypothesize that this crosstalk may hold valuable clues for biomarker discovery and the development of novel therapeutic strategies.

Indexed as

AutophagyExosomesNeoplasmsAnimalsCell CommunicationHumansNeovascularization, Pathologicangiogenesisautophagycancerexosomesmetastasistumor

Identifiers

PMID40318053
PMCPMC12141978

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.