Evidence map›Paper›PMID 40312304›Full record

ArticleBMC cancer2025

Integrating transcriptomic and metabolomic analyses to characterize the potential function of SLC1A5 in thyroid cancer.

Fengling Shan, Lan Wang, Xinyu Lu, Meihong Zhou, Zi Wang, Jingjing Lou, Xingdang Liu

Abstract read
In one paragraph

Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Fengling Shan *Department of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China.
Lan Wang *Department of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China.
Xinyu LuDepartment of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China.
Meihong ZhouDepartment of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China.
Zi WangDepartment of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China.
Jingjing LouDepartment of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China. 13586996644@163.com.
Xingdang LiuDepartment of Nuclear Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai, 201399, China. xingdliu@fudan.edu.cn.

Funding

Clinical research program of Health Industry of Shanghai Municipal Commission of Health 202150002Natural Science Foundation of China 82272042Research Grant for Health Science and Technology of Pudong Municipal Commission of Health committee of Shanghai PW2023B-15Specialty Feature Construction project of Pudong Health and Family Planning Commission of Shanghai PWYts2021-01the Scientific Research Foundation Provided by Pudong Hospital Affiliated to Fudan University No.YJRCJJ201907, No.YJYJRC202108, No.YJYJRC202101, No.Zdzk2020-14, No.Tszb2024-14, No.Tszb2024-15
6 · The paper itself

Abstract

backgroundAlanine Serine Cysteine transporter 2 (ASCT2/SLC1A5) is a key glutamine transporter in cancer cells and has been shown in a variety of cancers to promote tumor growth by reprogramming glutamine metabolism and altering the tumor microenvironment. However, the role in thyroid cancer remains unknown.

methodsTo investigate the expression and prognostic value of SLC1A5 in thyroid cancer using publically available databases, and to define the relationship with clinical characteristics. SLC1A5 expression in TPC-1 and B-CPAP was knocked down using SLC1A5 siRNA to investigate its effects on cell growth and apoptosis. Transcriptome sequencing and metabolite analysis were carried out in the SLC1A5 siRNA group to identify major transcriptomic or metabolite changes that could lead to apoptosis. In addition, we explored for the connection of SLC1A5 with the tumor microenvironment using algorithms like ESTIMATE and CIBERSORT.

resultsHigh SLC1A5 expression in THCA is related with a poor prognosis and advanced clinical stage. In vitro findings showed that SLC1A5 knockdown reduced THCA cell activity and accelerated apoptosis, and the results were consistent with the effect of SLC1A5 inhibitor GPNA. While RNA sequencing analysis revealed that NF-κb signaling was enhanced and oxidative phosphorylation levels were lowered. Metabolomics findings indicated that Glutathione and purine metabolism were dramatically affected in the SLC1A5 siRNA group. Furthermore, immune microenvironment study revealed that SLC1A5 had a positive correlation with the amount of CD4 + T memory-activated cells and T cell follicular helper cells.

conclusionSLC1A5 may be a possible target in THCA. Our findings indicate that DEGs and differential metabolites are mostly linked to numerous signaling pathways and immunological modulation, which may play an important role in SLC1A5 regulation of THCA development.

Indexed as

Amino Acid Transport System ASCMinor Histocompatibility AntigensThyroid NeoplasmsTranscriptomeApoptosisCell Line, TumorCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMetabolomicsPrognosisSignal TransductionTumor MicroenvironmentAmino Acid Transport System ASCMinor Histocompatibility AntigensSLC1A5 protein, humanMetabolomicsSLC1A5Thyroid cancerTranscriptomicsTumor microenvironment

Identifiers

PMID40312304
PMCPMC12044823

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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.