Evidence map›Paper›PMID 38606507›Full record

ReviewInternational journal of oncology2024

Beyond self‑eating: Emerging autophagy‑independent functions for the autophagy molecules in cancer (Review).

Giulia Tedesco, Manuela Santarosa, Roberta Maestro

Abstract readReview
In one paragraph

Review in International journal of oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. 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.

Giulia TedescoUnit of Oncogenetics and Functional Oncogenomics, CRO Aviano, National Cancer Institute, IRCCS, I‑33081 Aviano, Italy.
Manuela SantarosaUnit of Oncogenetics and Functional Oncogenomics, CRO Aviano, National Cancer Institute, IRCCS, I‑33081 Aviano, Italy.
Roberta MaestroUnit of Oncogenetics and Functional Oncogenomics, CRO Aviano, National Cancer Institute, IRCCS, I‑33081 Aviano, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a conserved catabolic process that controls organelle quality, removes misfolded or abnormally aggregated proteins and is part of the defense mechanisms against intracellular pathogens. Autophagy contributes to the suppression of tumor initiation by promoting genome stability, cellular integrity, redox balance and proteostasis. On the other hand, once a tumor is established, autophagy can support cancer cell survival and promote epithelial‑to‑mesenchymal transition. A growing number of molecules involved in autophagy have been identified. In addition to their key canonical activity, several of these molecules, such as ATG5, ATG12 and Beclin‑1, also exert autophagy‑independent functions in a variety of biological processes. The present review aimed to summarize autophagy‑independent functions of molecules of the autophagy machinery and how the activity of these molecules can influence signaling pathways that are deregulated in cancer progression.

Indexed as

NeoplasmsProteinsAutophagyBeclin-1HumansSignal TransductionBeclin-1Proteinsautophagyautophagy‑independentcancercancer progressioncell deathgenome instabilitymetastasisproliferationsurvival

Identifiers

PMID38606507
PMCPMC11087037

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.