Evidence map›Paper›PMID 32971884›Full record

ReviewCells2020

The Role of Chaperone-Mediated Autophagy in Cell Cycle Control and Its Implications in Cancer.

Marina Andrade-Tomaz, Izadora de Souza, Clarissa Ribeiro Reily Rocha, Luciana Rodrigues Gomes

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 80 citations in OpenAlex.

  1. Autophagy Defects and Mitochondrial Retention in Erythroid Diseases.International journal of molecular sciences · 2026
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  10. The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024
    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.

Marina Andrade-TomazDepartamento de Oncologia Clínica e Experimental, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04037-003, SP, Brazil.
Izadora de SouzaDepartamento de Oncologia Clínica e Experimental, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04037-003, SP, Brazil.
Clarissa Ribeiro Reily RochaDepartamento de Oncologia Clínica e Experimental, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04037-003, SP, Brazil.
Luciana Rodrigues GomesLaboratório de Ciclo Celular, Center of Toxins, Immune Response and Cell Signaling (CeTICS), Instituto Butantan, São Paulo 05503-001, SP, Brazil.
Universidade Federal de São Paulo · BRInstituto Butantan · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cell cycle involves a network of proteins that modulate the sequence and timing of proliferation events. Unregulated proliferation is the most fundamental hallmark of cancer; thus, changes in cell cycle control are at the heart of malignant transformation processes. Several cellular processes can interfere with the cell cycle, including autophagy, the catabolic pathway involved in degradation of intracellular constituents in lysosomes. According to the mechanism used to deliver cargo to the lysosome, autophagy can be classified as macroautophagy (MA), microautophagy (MI), or chaperone-mediated autophagy (CMA). Distinct from other autophagy types, CMA substrates are selectively recognized by a cytosolic chaperone, one-by-one, and then addressed for degradation in lysosomes. The function of MA in cell cycle control, and its influence in cancer progression, are already well-established. However, regulation of the cell cycle by CMA, in the context of tumorigenesis, has not been fully addressed. This review aims to present and debate the molecular mechanisms by which CMA can interfere in the cell cycle, in the context of cancer. Thus, cell cycle modulators, such as MYC, hypoxia-inducible factor-1 subunit alpha (HIF-1α), and checkpoint kinase 1 (CHK1), regulated by CMA activity will be discussed. Finally, the review will focus on how CMA dysfunction may impact the cell cycle, and as consequence promote tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticAutophagyCarcinogenesisCell Cycle CheckpointsChaperone-Mediated AutophagyCheckpoint Kinase 1Disease ProgressionHumansHypoxia-Inducible Factor 1, alpha SubunitLysosomesMolecular ChaperonesNeoplasmsNeoplastic Stem CellsProteolysisProto-Oncogene Proteins c-mycSignal TransductionCheckpoint Kinase 1CHEK1 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMolecular ChaperonesMYC protein, humanProto-Oncogene Proteins c-mycautophagycancerchaperone-mediated autophagy (CMA), cell cyclecheckpointshypoxia-inducible factor-1 subunit alpha (HIF-1α), checkpoint kinase 1 (CHK1)MYC

Identifiers

PMID32971884
PMCPMC7565978
OpenAlexW3088792484

What OpenQuestion 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 OpenQuestion graph.