Evidence map›Paper›PMID 35057861›Full record

ArticleHereditas2022

SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway.

Fangxing Wu, Gaoyun Xiong, Zejun Chen, Chenyang Lei, Qianqian Liu, Yundan Bai

Open access · goldAbstract read
In one paragraph

Article in Hereditas, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Open medicine (Warsaw, Poland) · 2024
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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.

Fangxing WuDepartment of Otolaryngology, Tongde Hospital of Zhejiang Province, No. 234 Gu Chui Road, Hangzhou, Zhejiang Province, China.
Gaoyun XiongDepartment of Otolaryngology, Tongde Hospital of Zhejiang Province, No. 234 Gu Chui Road, Hangzhou, Zhejiang Province, China.
Zejun ChenDepartment of General Medicine, Chengdu First People's Hospital, Chengdu, 610000, Sichuan Province, China.
Chenyang LeiDepartment of Otolaryngology, Tongde Hospital of Zhejiang Province, No. 234 Gu Chui Road, Hangzhou, Zhejiang Province, China.
Qianqian LiuDepartment of Respiratory and Critical Care Medicine, Chengdu First People's Hospital, Chengdu, 610000, Sichuan Province, China.
Yundan BaiDepartment of Health Management Medical Center, Chengdu First People's Hospital, Chengdu, 610000, Sichuan Province, China. byd1987@126.com.
Tongde Hospital of Zhejiang Province · CNFirst Affiliated Hospital of Chengdu Medical College · CN

Funding

medical scientific research project of chengdu health commission 2020016
6 · The paper itself

Abstract

objectiveThis study aimed to explore the mRNA and protein expression of SLC3A2 in laryngeal carcinoma cells and tissues, and functional regulatory mechanism of SLC3A2 in cell ferroptosis of laryngeal carcinoma.

methodsWe chose the key gene-SLC3A2 of DEGs from TCGA by bioinformatics analysis, and then we constructed stable knockdown of SLC3A2 in laryngeal carcinoma cells. MTT assay and clonogenic assay were used to determine cell viability and cell growth, respectively. The mRNA and protein expression were determined by RT-qPCR and western blotting, respectively. Xenograft tumor model was used to determine the role of SLC3A2 in tumor growth.

resultsThe results of limma analysis recovered that 92 genes were involved in both upregulated DEGs and high risk of poor prognosis, whereas 36 genes were involved in both downregulated DEGs and low risk of poor prognosis. Pathway enrichment analysis indicated that mTOR signaling pathway and ferroptosis exerted a role in regulating these intersection genes. Moreover, SLC3A2 is a key gene in ferroptosis in laryngeal carcinoma. SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells. Patients with high SLC3A2 expression exerted poor survival. SLC3A2 deficiency inhibited cell proliferation and foci formation. Furthermore, knockdown of SLC3A2 expression induced the efficacy of ferroptosis and suppressed ferroptosis related proteins expression. Mechanically, SLC3A2 deficiency facilitated ferroptosis through upregulating the expression of mTOR and P70S6K, whereas inhibited p-mTOR and p-P70S6K expression in laryngeal carcinoma cells. SLC3A2 deficiency inhibited tumorigenesis in nude mice.

conclusionOur study suggests that SLC3A2 negatively regulates ferroptosis through mTOR pathway in laryngeal carcinoma.

Indexed as

CarcinomaFerroptosisAnimalsCell ProliferationFusion Regulatory Protein 1, Heavy ChainHumansLaryngeal NeoplasmsMiceMice, NudeTOR Serine-Threonine KinasesFusion Regulatory Protein 1, Heavy ChainMTOR protein, humanSLC3A2 protein, humanSlc3A2 protein, mouseTOR Serine-Threonine KinasesCell proliferationFerroptosisLaryngeal carcinomamTORSLC3A2

Identifiers

PMID35057861
PMCPMC8772086
OpenAlexW4206241787

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.