Evidence map›Paper›PMID 36639654›Full record

ArticleCancer cell international2023

Heat shock protein 27 deficiency promotes ferrous ion absorption and enhances acyl-Coenzyme A synthetase long-chain family member 4 stability to promote glioblastoma cell ferroptosis.

Kai Zhang, Yue Wu, Guangliang Chen, Hao Wang, Yongsheng Liu, Youxin Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
7.8field-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

16 citing papers in PubMed, 28 citations in OpenAlex.

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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 2 institutions in 1 country.

Kai Zhang *Department of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Yue Wu *Department of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Guangliang ChenDepartment of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Hao WangDepartment of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Yongsheng LiuDepartment of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Youxin ZhouDepartment of Neurosurgery, Laboratory of Brain and Nerve Research, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China. brain_lab@suda.edu.cn.
First Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma is one of the malignant tumors of the central nervous system with high lethality, high disability and low survival rate. Effective induction of its death is one of the existing challenges. In recent studies, heat shock protein 27 (HSP27) has been shown to be associated with ferroptosis; therefore, targeting HSP27 may be a potential therapeutic approach for GBM.

methodsImmunohistochemistry and western blot analysis were used to detect the expression of HSP27 in GBM tissues. CCK8, plate clone formation assay, EdU proliferation assay for cell proliferation ability, PI, LDH release assay for cell viability. Reactive oxygen, iron levels, and mitochondrial potential for HSP27 silencing were assayed for ferrotosis in vitro. Western blotting and IP were used to verify the relationship between HSP27 and ACSL4. The effect of knockdown of HSP27 on tumor growth capacity was assessed in an intracranial xenograft model.

resultsHSP27 was significantly highly expressed in GBM. In vitro experiments, knockdown of HSP27 significantly induced ferroptosis in GBM cells. IP and western blot demonstrated a sumo-ization link between HSP27 and ACSL4. In vivo experiments, HSP27 deficiency retarded tumor growth rate by promoting ferroptosis.

conclusionsHSP27 deficiency promotes GBM ferroptosis. Targeting HSP27 may serve as a new direction for GBM treatment.

Indexed as

ACSL4Fe2+FerroptosisGBMHSP27ROSSUMO

Identifiers

PMID36639654
PMCPMC9840324
OpenAlexW4315874480

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Registered trials

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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.