Evidence map›Paper›PMID 27171435›Full record

ArticlePloS one2016

Erastin Disrupts Mitochondrial Permeability Transition Pore (mPTP) and Induces Apoptotic Death of Colorectal Cancer Cells.

Haizhong Huo, Zhiyuan Zhou, Jian Qin, Wenyong Liu, Bing Wang, Yan Gu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

65 citing papers in PubMed, 118 citations in OpenAlex.

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  16. Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications.Apoptosis : an international journal on programmed cell death · 2024
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  18. Article
  19. Article
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5 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

6 authors at 2 institutions in 1 country.

Haizhong HuoDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Zhiyuan ZhouDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Jian QinDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Wenyong LiuDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Bing WangDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Yan GuDepartment of General Surgery, The Ninth People's Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We here evaluated the potential anti-colorectal cancer activity by erastin, a voltage-dependent anion channel (VDAC)-binding compound. Our in vitro studies showed that erastin exerted potent cytotoxic effects against multiple human colorectal cancer cell lines, possibly via inducing oxidative stress and caspase-9 dependent cell apoptosis. Further, mitochondrial permeability transition pore (mPTP) opening was observed in erastin-treated cancer cells, which was evidenced by VDAC-1 and cyclophilin-D (Cyp-D) association, mitochondrial depolarization, and cytochrome C release. Caspase inhibitors, the ROS scavenger MnTBAP, and mPTP blockers (sanglifehrin A, cyclosporin A and bongkrekic acid), as well as shRNA-mediated knockdown of VDAC-1, all significantly attenuated erastin-induced cytotoxicity and apoptosis in colorectal cancer cells. On the other hand, over-expression of VDAC-1 augmented erastin-induced ROS production, mPTP opening, and colorectal cancer cell apoptosis. In vivo studies showed that intraperitoneal injection of erastin at well-tolerated doses dramatically inhibited HT-29 xenograft growth in severe combined immunodeficient (SCID) mice. Together, these results demonstrate that erastin is cytotoxic and pro-apoptotic to colorectal cancer cells. Erastin may be further investigated as a novel anti-colorectal cancer agent.

Indexed as

AnimalsApoptosisCaspase 3Caspase 9Cell Line, TumorCell ProliferationColorectal NeoplasmsHT29 CellsHumansMice, SCIDMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePiperazinesReactive Oxygen SpeciesVoltage-Dependent Anion Channel 1Xenograft Model Antitumor AssaysCaspase 3Caspase 9erastinMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePiperazinesReactive Oxygen SpeciesVDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID27171435
PMCPMC4865238
OpenAlexW2384698380

What OpenQuestion holds

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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.