Evidence map›Paper›PMID 37914960›Full record

ArticleBreast cancer (Tokyo, Japan)2024

SLC38A5 promotes glutamine metabolism and inhibits cisplatin chemosensitivity in breast cancer.

Xiaowei Shen, Ganggang Wang, Hua He, Ping Shang, Bin Yan, Xiaoliang Wang, Weixing Shen

Abstract read
PubMed Publisher
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 19 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

7 authors at 1 institution in 1 country.

Xiaowei Shen *Department of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China. damonsxw@outlook.com.ORCID http://orcid.org/0000-0002-2729-2432
Ganggang Wang *Department of Hepatobiliary Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Hua He *Department of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China.
Ping ShangDepartment of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China.
Bin YanDepartment of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China.
Xiaoliang WangDepartment of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China.
Weixing ShenDepartment of General Surgery, QingPu Branch of Zhongshan Hospital Affiliated to Fudan University, QingPu District Central Hospital Shanghai, No. 1158, Gong Yuan Dong Road, Shanghai, 201700, China.
Fudan University · CN

Funding

Shanghai Health Care Commission 202040065Shanghai Natural Science Foundation 20ZR1411900
6 · The paper itself

Abstract

backgroundSolute carrier family 38 member 5 (SLC38A5), as an amino acid transporter, play a vital role in cellular biological processes. In this study, we analyzed the function of SLC38A5 and its potential mechanism in breast cancer (BC) progression.

methodsThe expression of SLC38A5 in cancer and adjacent-normal tissues was analyzed by qRT-PCR and Western blot, and its correlation with patient prognosis was analyzed. The immunohistochemical staining of cancer tissues and adjacent-normal tissues was performed on SLC38A5-positive specimens. BC mice were successfully applied to examine the role of SLC38A5 on tumor proliferation using the CCK-8 assay. In BC cells and mouse tumor tissues, SLC38A5 and PCNA expression were determined by Western blotting.

resultsThe study found that SLC38A5 was highly expressed in BC patients and associated with a poor survival. SLC38A5 silencing inhibited BC cell viability and glutamine uptake. In addition, SLC38A5 overexpression promoted BC cell viability via the glutamine metabolism. SLC38A5 inhibited cisplatin chemosensitivity in BC cells. Importantly, SLC38A5 silencing inhibited tumor growth in vivo.

conclusionOur findings suggest that SLC38A5 enhances BC cell viability by glutamine metabolism, inhibits the chemical sensitivity of cisplatin in BC cells, and promotes tumor growth, emphasizing the clinical relevance of SLC38A5 in BC management as a novel potential therapeutic target.

Indexed as

Amino Acid Transport Systems, NeutralBreast NeoplasmsAnimalsCell Line, TumorCell ProliferationCisplatinFemaleGlutamineHumansMiceAmino Acid Transport Systems, NeutralCisplatinGlutamineSLC38A5 protein, humanBreast cancerCisplatin chemosensitivityGlutamine metabolismSLC38A5

Identifiers

PMID37914960
OpenAlexW4388229162

What OpenQuestion holds

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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.