Evidence map›Paper›PMID 26448608›Full record

ArticleJournal of cellular biochemistry2016

Autophagy-Mediated Degradation of IAPs and c-FLIP(L) Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24.

Jennings Xu, Xiuling Xu, Shaoqing Shi, Qiong Wang, Bryanna Saxton, Weiyang He, Xin Gou, Jun-Ho Jang, Toru Nyunoya, Xia Wang and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  5. The interplay of autophagy and non-apoptotic cell death pathways.International review of cell and molecular biology · 2020
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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

13 authors at 8 institutions in 2 countries.

Jennings XuMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Xiuling XuMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Shaoqing ShiMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Qiong WangMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Bryanna SaxtonMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Weiyang HeDepartment of Urology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, 510182, P.R. China.
Xin GouDepartment of Urology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, 510182, P.R. China.
Jun-Ho JangLaboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Toru NyunoyaLaboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Xia WangLaboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Chengguo XingDepartment of Medicinal Chemistry, University of Minnesota, Minneapolis, 55455, Minnesota.
Lin ZhangLaboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Yong LinMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.
Lovelace Respiratory Research Institute · USSichuan University · CNWest China Second University Hospital of Sichuan University · CNChongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNNew Mexico VA Health Care System · USUniversity of Minnesota System · USUniversity of New Mexico · US

Funding

Bridging Inflammation and Cigarette Smoke-associated Lung Carcinogenesis by MUC1R01ES017328 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2010 to 2014
$2.2M
Mechanisms of Anticancer Agents Selective against Drug Resistant LeukemiaR01CA163864 · NCI · UNIVERSITY OF MINNESOTA · PI XING, CHENGGUO · 2012 to 2016
$1.5M
Developing a Post-carcinogen Lung Cancer Chemopreventive AgentR01CA142649 · NCI · UNIVERSITY OF MINNESOTA · PI XING, CHENGGUO · 2010 to 2014
$1.0M
Role of DNA Repair in COPDI01CX001048 · VA · VETERANS HEALTH ADMINISTRATION · PI NYUNOYA, TORU · 2015 to 2017
–
CSRD VA I01 CX001048NCI NIH HHS R01 CA142649NCI NIH HHS R01CA142649NCI NIH HHS R01 CA163864NIEHS NIH HHS R01 ES017328NIEHS NIH HHS R01ES017328
6 · The paper itself

Abstract

Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone-24 (Chal-24), and TNF-related apoptosis-inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal-24 treatment significantly enhanced TRAIL-induced activation of caspase-8 and caspase-3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan-caspase inhibitor z-VAD-fmk. Chal-24 and TRAIL combination suppressed expression of cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein large (c-FLIP(L)) and cellular inhibitor of apoptosis proteins (c-IAPs), and ectopic expression of c-FLIP(L) and c-IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal-24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal-24 and TRAIL combination, which was associated with attenuation of c-FLIP(L) and c-IAPs degradation. Altogether, these results suggest that Chal-24 potentiates the anticancer activity of TRAIL through autophagy-mediated degradation of c-FLIP(L) and c-IAPs, and that combination of Chal-24 and TRAIL could be an effective approach in improving chemotherapy efficacy.

Indexed as

A549 CellsAmino Acid Chloromethyl KetonesApoptosisAutophagyBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 3Caspase 8Caspase InhibitorsCell Line, TumorCell SurvivalChalconesDose-Response Relationship, DrugDrug SynergismHumansInhibitor of Apoptosis Proteins3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-oneAmino Acid Chloromethyl Ketonesbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 3Caspase 8Caspase InhibitorsCFLAR protein, humanChalconesInhibitor of Apoptosis ProteinsTNF-Related Apoptosis-Inducing LigandAPOPTOSISAUTOPHAGYc-FLIPCHAL-24c-IAPTRAIL

Identifiers

PMID26448608
PMCPMC4894717
OpenAlexW1847186775

What OpenQuestion holds

Textmetadata
LicenceTDM
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.