Evidence map›Paper›PMID 24722279›Full record

ArticlePloS one2014

Autophagy inhibitor LRPPRC suppresses mitophagy through interaction with mitophagy initiator Parkin.

Jing Zou, Fei Yue, Wenjiao Li, Kun Song, Xianhan Jiang, Jinglin Yi, Leyuan Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Guideline
  4. Article
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  7. Review
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  20. The NADMechanisms of ageing and development · 2020
    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

7 authors at 2 institutions in 2 countries.

Jing ZouCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America; Jiangxi Research Institute of Ophthalmology and Visual Sciences, The Affiliated Eye Hospital of Nanchang University, Nanchang, Jiangxi, China.
Fei YueCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America.
Wenjiao LiCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America.
Kun SongCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America.
Xianhan JiangCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America.
Jinglin YiJiangxi Research Institute of Ophthalmology and Visual Sciences, The Affiliated Eye Hospital of Nanchang University, Nanchang, Jiangxi, China.
Leyuan LiuCenter for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas, United States of America.
Texas A&M Health Science Center · USNanchang University · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Roles of C19ORF5 and LRPPRC in Autophagy and Tumor SuppressionR01CA142862 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI LIU, LEYUAN · 2010 to 2014
$1.2M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA142862
6 · The paper itself

Abstract

Autophagy plays an important role in tumorigenesis. Mitochondrion-associated protein LRPPRC interacts with MAP1S that interacts with LC3 and bridges autophagy components with microtubules and mitochondria to affect autophagy flux. Dysfunction of LRPPRC and MAP1S is associated with poor survival of ovarian cancer patients. Furthermore, elevated levels of LRPPRC predict shorter overall survival in patients with prostate adenocarcinomas or gastric cancer. To understand the role of LRPPRC in tumor development, previously we reported that LRPPRC forms a ternary complex with Beclin 1 and Bcl-2 to inhibit autophagy. Here we further show that LRPPRC maintains the stability of Parkin that mono-ubiquitinates Bcl-2 to increase Bcl-2 stability to inhibit autophagy. Under mitophagy stress, Parkin translocates to mitochondria to cause rupture of outer mitochondrial membrane and bind with exposed LRPPRC. Consequently, LRPPRC and Parkin help mitochondria being engulfed in autophagosomes to be degraded. In cells under long-term mitophagy stress, both LRPPRC and Parkin become depleted coincident with disappearance of mitochondria and final autophagy inactivation due to depletion of ATG5-ATG12 conjugates. LRPPRC functions as a checkpoint protein that prevents mitochondria from autophagy degradation and impact tumorigenesis.

Indexed as

Apoptosis Regulatory ProteinsAutophagyBeclin-1CarcinogenesisHeLa CellsHumansMembrane ProteinsMitochondriaMitophagyNeoplasm ProteinsPhagosomesProto-Oncogene Proteins c-bcl-2Ubiquitin-Protein LigasesApoptosis Regulatory ProteinsBCL2 protein, humanBeclin-1BECN1 protein, humanLRPPRC protein, humanMembrane ProteinsNeoplasm Proteinsparkin proteinProto-Oncogene Proteins c-bcl-2Ubiquitin-Protein Ligases

Identifiers

PMID24722279
PMCPMC3983268
OpenAlexW2121053966

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.