Evidence map›Paper›PMID 22708544›Full record

ArticleBritish journal of pharmacology2012

Inhibition of lysosome degradation on autophagosome formation and responses to GMI, an immunomodulatory protein from Ganoderma microsporum.

I-Lun Hsin, Gwo-Tarng Sheu, Ming-Shiou Jan, Hai-Lun Sun, Tzu-Chin Wu, Ling-Yen Chiu, Ko-Huang Lue, Jiunn-Liang Ko

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Review
  5. Quantitative Proteomic Analysis of Macrophages Infected withInternational journal of molecular sciences · 2024
    Article
  6. Article
  7. Ganoderma immunomodulatory proteins: mushrooming functional FIPs.Applied microbiology and biotechnology · 2022
    Review
  8. Article
  9. Article
  10. GMI, an Immunomodulatory Peptide fromInternational journal of molecular sciences · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Proteomic Analysis of Mouse Brain Subjected to Spaceflight.International journal of molecular sciences · 2018
    Article
  15. Review
  16. Review
  17. Article
  18. Frontiers in pharmacology · 2018
    Review
  19. Review
  20. 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 2 institutions in 1 country.

I-Lun HsinInstitute of Medical and Molecular Toxicology, Chung Shan Medical University, Taichung, Taiwan.
Gwo-Tarng Sheu
Ming-Shiou Jan
Hai-Lun Sun
Tzu-Chin Wu
Ling-Yen Chiu
Ko-Huang Lue
Jiunn-Liang Ko
Chung Shan Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAutophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death. EXPERIMENTAL APPROACH: Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. KEY

resultsLysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H(+)-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS: We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.

Indexed as

GanodermaAutophagyCell Line, TumorChloroquineFungal ProteinsGene SilencingHumansImmunologic FactorsLysosomesMacrolidesPhagosomesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVacuolar Proton-Translocating ATPasesATP6V0A1 protein, humanbafilomycin A1ChloroquineFungal ProteinsImmunologic FactorsMacrolidesMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVacuolar Proton-Translocating ATPases

Identifiers

PMID22708544
PMCPMC3504994
OpenAlexW1928236782

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.