Evidence map›Paper›PMID 26188905›Full record

ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Anticancer drugs for the modulation of endoplasmic reticulum stress and oxidative stress.

Ammad Ahmad Farooqi, Kun-Tzu Li, Sundas Fayyaz, Yung-Ting Chang, Muhammad Ismail, Chih-Chuang Liaw, Shyng-Shiou F Yuan, Jen-Yang Tang, Hsueh-Wei Chang

Open access · hybridAbstract readReview
In one paragraph

Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 126 citations in OpenAlex.

  1. Sulfur Vacancy-Enriched CuAngewandte Chemie (International ed. in English) · 2026
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  6. Anti-cancer effect ofRPS pharmacy and pharmacology reports · 2023
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  7. Review
  8. Article
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  17. Review
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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

9 authors at 7 institutions in 2 countries.

Ammad Ahmad FarooqiInstitute of Biomedical and Genetic Engineering (IBGE), KRL Hospital, Islamabad, Pakistan, ammadfarooqi@rlmclahore.com.
Kun-Tzu Li
Sundas Fayyaz
Yung-Ting Chang
Muhammad Ismail
Chih-Chuang Liaw
Shyng-Shiou F Yuan
Jen-Yang Tang
Hsueh-Wei Chang
Institute of Biomedical and Genetic Engineering · PKNational Sun Yat-sen University · TWAcademia Sinica · TWKaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWKaohsiung Municipal Ta-Tung Hospital · TWRashid Latif Medical College · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prior research has demonstrated how the endoplasmic reticulum (ER) functions as a multifunctional organelle and as a well-orchestrated protein-folding unit. It consists of sensors which detect stress-induced unfolded/misfolded proteins and it is the place where protein folding is catalyzed with chaperones. During this folding process, an immaculate disulfide bond formation requires an oxidized environment provided by the ER. Protein folding and the generation of reactive oxygen species (ROS) as a protein oxidative byproduct in ER are crosslinked. An ER stress-induced response also mediates the expression of the apoptosis-associated gene C/EBP-homologous protein (CHOP) and death receptor 5 (DR5). ER stress induces the upregulation of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) receptor and opening new horizons for therapeutic research. These findings can be used to maximize TRAIL-induced apoptosis in xenografted mice. This review summarizes the current understanding of the interplay between ER stress and ROS. We also discuss how damage-associated molecular patterns (DAMPs) function as modulators of immunogenic cell death and how natural products and drugs have shown potential in regulating ER stress and ROS in different cancer cell lines. Drugs as inducers and inhibitors of ROS modulation may respectively exert inducible and inhibitory effects on ER stress and unfolded protein response (UPR). Reconceptualization of the molecular crosstalk among ROS modulating effectors, ER stress, and DAMPs will lead to advances in anticancer therapy.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsEndoplasmic Reticulum StressHumansMiceNeoplasmsOxidative StressProtein FoldingReactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTranscription Factor CHOPAntineoplastic AgentsDDIT3 protein, humanReactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTranscription Factor CHOP

Identifiers

PMID26188905
PMCPMC4546701
OpenAlexW908095114

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.