Evidence map›Paper›PMID 26029922›Full record

ArticlePloS one2015

Autophagy-Regulated ROS from Xanthine Oxidase Acts as an Early Effector for Triggering Late Mitochondria-Dependent Apoptosis in Cathepsin S-Targeted Tumor Cells.

Chien-Chang Huang, Cheng-Che Lee, Hsiao-Han Lin, Mei-Chi Chen, Chun-Cheng Lin, Jang-Yang Chang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  16. Redox regulation of autophagy in skeletal muscle.Free radical biology & medicine · 2016
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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

6 authors at 3 institutions in 1 country.

Chien-Chang HuangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, ROC.
Cheng-Che LeeNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, ROC.
Hsiao-Han LinNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, ROC; The Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Mei-Chi ChenNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, ROC.
Chun-Cheng LinDepartment of Chemistry, National Tsing Hua University, Hsinchu, Taiwan, ROC.
Jang-Yang ChangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, ROC; Division of Hematology and Oncology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC; Institute of Molecular Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
National Health Research Institutes · TWNational Cheng Kung University · TWNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cathepsin S (CTSS), which is highly expressed in various malignant tumor cells, has been proposed to promote tumor progression, migration, and invasion. CTSS inhibition not only blocks tumor cell invasion and endothelial tube formation but also induces cellular cytotoxicity. In our previous studies, we have observed that CTSS inhibition induces autophagy, which is responsible for up-regulating xanthine oxidase for early ROS generation and consequent cell death. However, whether the autophagy-regulated early ROS triggers apoptosis remains unclear. We conducted a long-term follow-up study to investigate the relationship between early autophagy and late mitochondria-dependent apoptosis. We demonstrated that early ROS generation is critical for mitochondria damage and the activation of intrinsic apoptotic pathway. Attenuating the early ROS level diminished later mitochondrial damage and downstream apoptotic signaling. Collectively, mitochondria-dependent apoptosis is regulated by autophagy-regulated early ROS, which serves as an early effector that triggers mitochondrial signaling for late apoptosis. The data emphasize the essential role of autophagy-regulated early ROS in triggering late apoptotic signaling.

Indexed as

ApoptosisAutophagyCaspase 3Caspase 9CathepsinsCell Line, TumorHumansMitochondriaMolecular Targeted TherapyProtease InhibitorsReactive Oxygen SpeciesRespiratory BurstSignal TransductionXanthine OxidaseCaspase 3Caspase 9cathepsin SCathepsinsProtease InhibitorsReactive Oxygen SpeciesXanthine Oxidase

Identifiers

PMID26029922
PMCPMC4452096
OpenAlexW630216016

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.