Evidence map›Paper›PMID 34074205›Full record

ArticleAutophagy2022

Silencing PEX26 as an unconventional mode to kill drug-resistant cancer cells and forestall drug resistance.

Michael S Dahabieh, Fan Huang, Christophe Goncalves, Raúl Ernesto Flores González, Sathyen Prabhu, Alicia Bolt, Erminia Di Pietro, Elie Khoury, John Heath, Zi Yi Xu and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Mammalian pexophagy at a glance.Journal of cell science · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?Frontiers in cell and developmental biology · 2021
    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

17 authors at 3 institutions in 1 country.

Michael S DahabiehLady Davis Institute, McGill University, Montréal, Canada.
Fan HuangLady Davis Institute, McGill University, Montréal, Canada.ORCID 0000-0002-3850-5317
Christophe GoncalvesLady Davis Institute, McGill University, Montréal, Canada.
Raúl Ernesto Flores GonzálezLady Davis Institute, McGill University, Montréal, Canada.
Sathyen PrabhuLady Davis Institute, McGill University, Montréal, Canada.
Alicia BoltLady Davis Institute, McGill University, Montréal, Canada.
Erminia Di PietroDepartment of Human Genetics and Pediatrics, Research Institute of McGill University Children's Hospital, Montréal, Canada.
Elie KhouryLady Davis Institute, McGill University, Montréal, Canada.
John HeathLady Davis Institute, McGill University, Montréal, Canada.
Zi Yi XuLady Davis Institute, McGill University, Montréal, Canada.
Joelle Rémy-SarrazinLady Davis Institute, McGill University, Montréal, Canada.ORCID 0000-0002-3081-3307
Koren K MannLady Davis Institute, McGill University, Montréal, Canada.
Alexandre OrthweinLady Davis Institute, McGill University, Montréal, Canada.
François-Michel BoisvertDépartement d'anatomie et de biologie cellulaire, Université de Sherbrooke, Sherbrooke, Canada.
Nancy BravermanDepartment of Human Genetics and Pediatrics, Research Institute of McGill University Children's Hospital, Montréal, Canada.
Wilson H MillerLady Davis Institute, McGill University, Montréal, Canada.
Sonia V Del RincónLady Davis Institute, McGill University, Montréal, Canada.
McGill University · CAMontreal Children's Hospital · CAUniversité de Sherbrooke · CA

Funding

CIHR MOP-142281CIHR PJT-156269CIHR PJT-162260
6 · The paper itself

Abstract

Promoting the macroautophagy/autophagy-mediated degradation of specific proteins and organelles can potentially be utilized to induce apoptosis in cancer cells or sensitize tumor cells to therapy. To examine this concept, we enriched for autophagosomes from histone deacetylase inhibitor (HDACi)-sensitive U937 lymphoma cells and isogenic HDACi-resistant cells. Mass spectrometry on autophagosome-enriched fractions revealed that HDACi-resistant cells undergo elevated pexophagy, or autophagy of the peroxisome, an organelle that supports tumor growth. To disturb peroxisome homeostasis, we enhanced pexophagy in HDACi-resistant cells via genetic silencing of peroxisome exportomer complex components (

Indexed as

AutophagyMelanomaATPases Associated with Diverse Cellular ActivitiesDrug ResistanceFatty AcidsHumansMembrane ProteinsPeroxisomesTOR Serine-Threonine KinasesATPases Associated with Diverse Cellular ActivitiesFatty AcidsMembrane ProteinsPEX1 protein, humanPEX26 protein, humanPEX6 protein, humanTOR Serine-Threonine KinasesApoptosisautophagyexportomerperoxisomepexophagy

Identifiers

PMID34074205
PMCPMC9037551
OpenAlexW3164752133

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.