Evidence map›Paper›PMID 31464035›Full record

ArticleCancer science2019

Targeted exosome-encapsulated erastin induced ferroptosis in triple negative breast cancer cells.

Mengyu Yu, Chengcheng Gai, Zihaoran Li, Dejun Ding, Jie Zheng, Weifen Zhang, Shijun Lv, Wentong Li

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 2 pooled it
32.1field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 2 syntheses or guidelines pooled it, 342 citations in OpenAlex.

  1. Pooled it
  2. Exosomes in pathogenesis, diagnosis, and therapy of ischemic stroke.Frontiers in bioengineering and biotechnology · 2022
    Pooled it
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136 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Mengyu YuDepartment of Pathology, Weifang Medical University, Weifang, China.
Chengcheng GaiDepartment of Pathology, Weifang Medical University, Weifang, China.
Zihaoran LiDepartment of Pathology, Weifang Medical University, Weifang, China.
Dejun DingDepartment of Pharmacology, Weifang Medical University, Weifang, China.
Jie ZhengDepartment of Pathology, Weifang Medical University, Weifang, China.ORCID https://orcid.org/0000-0003-1526-0617
Weifen ZhangCollaborative Innovation Center for Target Drug Delivery System, Weifang Medical University, Weifang, China.
Shijun LvDepartment of Pathology, Weifang Medical University, Weifang, China.
Wentong LiDepartment of Pathology, Weifang Medical University, Weifang, China.ORCID https://orcid.org/0000-0002-8855-2162
Weifang Medical University · CN

Funding

National Natural Science Foundation of China 81472365National Natural Science Foundation of China 81774125National Natural Science Foundation of China 81802474
6 · The paper itself

Abstract

Ferroptosis is an iron-dependent, lipid peroxide-driven cell death caused by inhibition of the cystine/glutamate transporter, which is of importance for the survival of triple-negative breast cancer (TNBC) cells. Erastin is a low molecular weight chemotherapy drug that induces ferroptosis; however, poor water solubility and renal toxicity have limited its application. Exosomes, as drug delivery vehicles with low immunogenicity, high biocompatibility and high efficiency, have attracted increasing attention in recent years. Herein, we developed a formulation of erastin-loaded exosomes labeled with folate (FA) to form FA-vectorized exosomes loaded with erastin (erastin@FA-exo) to target TNBC cells with overexpression of FA receptors. The characterization, drug release, internalization and anti-tumor effect in vitro of erastin@FA-exo were determined. Erastin@FA-exo could increase the uptake efficiency of erastin into MDA-MB-231 cells; compared with erastin@exo and free erastin, erastin@FA-exo has a better inhibitory effect on the proliferation and migration of MDA-MB-231 cells. Furthermore, erastin@FA-exo promoted ferroptosis with intracellular depletion of glutathione and reactive oxygen species overgeneration. Western blot analyses revealed that erastin@FA-exo suppressed expression of glutathione peroxidase 4 (GPX4) and upregulated expression of cysteine dioxygenase (CDO1). We conclude that targeting and biocompatibility of exosome-based erastin preparations provide an innovative and powerful delivery platform for anti-cancer therapy.

Indexed as

Cell DeathCell Line, TumorCell MovementCell ProliferationCell SurvivalCysteine DioxygenaseDrug Delivery SystemsExosomesFolic AcidGene Expression Regulation, NeoplasticGlutathione PeroxidaseHumansPhospholipid Hydroperoxide Glutathione PeroxidasePiperazinesReactive Oxygen SpeciesTriple Negative Breast NeoplasmsCDO1 protein, humanCysteine DioxygenaseerastinFolic AcidGlutathione PeroxidasePhospholipid Hydroperoxide Glutathione PeroxidasePiperazinesReactive Oxygen Specieserastinexosomesferroptosisreactive oxygen speciestriple negative breast cancer

Identifiers

PMID31464035
PMCPMC6778638
OpenAlexW2970433432

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.