Evidence map›Paper›PMID 37978473›Full record

ArticleBMC cancer2023

Knockdown of SLC39A14 inhibits glioma progression by promoting erastin-induced ferroptosis SLC39A14 knockdown inhibits glioma progression.

Yunwen Zhang, Xinghai Wu, Jiyong Zhu, Ruibin Lu, Yian Ouyang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 22 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

5 authors at 3 institutions in 1 country.

Yunwen ZhangDepartment of Neurosurgery, First Clinical Medical College of Gannan Medical University, No.1 Xueyuan Road, Zhanggong District, Ganzhou City, 341000, Jiangxi Province, China.
Xinghai WuDepartment of Neurosurgery, Zhangye People's Hospital Affiliated to Hexi University, No. 67 Xihuan Road, Ganzhou District, Zhangye City, 734000, Gansu Province, China.
Jiyong ZhuDepartment of Neurosurgery, Guilin Municipal Hospital of Traditional Chinese Medicine, Guangxi Zhuang Autonomous Region, No. 2 Lingui Road, Xiangshan District, Guilin City, 541002, China.
Ruibin LuDepartment of Neurosurgery, First Clinical Medical College of Gannan Medical University, No.1 Xueyuan Road, Zhanggong District, Ganzhou City, 341000, Jiangxi Province, China.
Yian OuyangDepartment of Neurosurgery, First Affiliated Hospital of Gannan Medical University, No.23 Qingnian Road, Zhanggong District, Ganzhou City, 341000, Jiangxi Province, China. ouyangyian2023@163.com.
Gannan Medical University · CNFirst Affiliated Hospital of Gannan Medical University · CNHexi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFerroptosis is a newly classified form of regulated cell death with implications in various tumor progression pathways. However, the roles and mechanisms of ferroptosis-related genes in glioma remain unclear.

methodsBioinformatics analysis was employed to identify differentially expressed ferroptosis-related genes in glioma. The expression levels of hub genes were assessed using real-time reverse transcriptase-polymerase chain reaction (RT-qPCR). To explore the role of SLC39A14 in glioma, a series of in vitro assays were conducted, including cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, wound healing, and Transwell assays. Enzyme-linked immunosorbent assay (ELISA) was utilized to measure the levels of indicators associated with ferroptosis. Hematoxylin-eosin (HE) and immunohistochemistry (IHC) staining were performed to illustrate the clinicopathological features of the mouse transplantation tumor model. Additionally, Western blot analysis was used to assess the expression of the cGMP-PKG pathway-related proteins.

resultsSeven ferroptosis-related hub genes, namely SLC39A14, WWTR1, STEAP3, NOTCH2, IREB2, HIF1A, and FANCD2, were identified, all of which were highly expressed in glioma. Knockdown of SLC39A14 inhibited glioma cell proliferation, migration, and invasion, while promoting apoptosis. Moreover, SLC39A14 knockdown also facilitated erastin-induced ferroptosis, leading to the suppression of mouse transplantation tumor growth. Mechanistically, SLC39A14 knockdown inhibited the cGMP-PKG signaling pathway activation.

conclusionSilencing SLC39A14 inhibits ferroptosis and tumor progression, potentially involving the regulation of the cGMP-PKG signaling pathway.

Indexed as

Cation Transport ProteinsFerroptosisGliomaAnimalsApoptosisCell Line, TumorCell ProliferationMicePiperazinesCation Transport ProteinserastinPiperazinesSLC39A14 protein, mouseFerroptosisGliomaSLC39A14The cGMP-PKG signaling pathway

Identifiers

PMID37978473
PMCPMC10655456
OpenAlexW4388767327

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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.