Evidence map›Paper›PMID 40031971›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

[SLC1A5 overexpression accelerates progression of hepatocellular carcinoma by promoting M2 polarization of macrophages].

Jinhua Zou, Hui Wang, Dongyan Zhang

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

1 citing paper in PubMed.

  1. Article
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

3 authors.

Jinhua ZouDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Hui WangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Dongyan ZhangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Funding

National Natural Science Foundation of China 82272719
6 · The paper itself

Abstract

objectivesTo investigate the clinical significance of SLC1A5 overexpression in pan-cancer and its mechanism for promoting hepatocellular carcinoma (HCC) progression.

methodsWe analyzed the correlation of SLC1A5 expression with clinical stage, lymph node metastasis and prognosis in pan-cancer using TCGA and ICGC datasets and explored its association with immune cell infiltration using EPIC, CIBERSORT, and TIMER algorithms. In HCC cell lines, the effects of lentivirus-mediated SLC1A5 overexpression or RNA interference on cell proliferation were examined using CCK-8 assay, and the growth of HCC cell xenografts overexpressing SLC1A5 was observed in nude mice. The effects of SLC1A5 overexpression or silencing in HCC cells on macrophage polarization were evaluated in a cell co-culture system.

resultsSLC1A5 was mainly localized on cell membrane and was highly expressed in most cancers in association with clinical stage, lymph node metastasis and poor prognosis. SLC1A5 expression was positively correlated with immunity score in 13 cancer types, especially in low-grade glioma (LGG), LIHC and thyroid cancer. SLC1A5 was positively correlated with macrophage infiltration level in LGG and LIHC but negatively correlated with macrophage infiltration in 5 cancers including lung squamous carcinoma, pancreatic carcinoma, and gastric carcinoma. Patients with SLC1A5 overexpression and high level of M2 macrophage infiltration had the worst survival outcomes. SLC1A5 was correlated with immunosuppression-related genes, cytokines, and cytokine receptors, which was the most obvious in LGG and LIHC. SLC1A5 was highly expressed in different HCC cell lines, and its overexpression promoted HCC cell proliferation both

conclusionsSLC1A5 expression level is correlated with clinical stage, lymph node metastasis, prognosis, and immune cell infiltration in most cancers, and its overexpression promotes HCC progression by inhibiting T-cell function

Indexed as

Amino Acid Transport System ASCCarcinoma, HepatocellularLiver NeoplasmsMacrophagesAnimalsCell Line, TumorCell ProliferationDisease ProgressionHumansLymphatic MetastasisMiceMice, NudeMinor Histocompatibility AntigensPrognosisAmino Acid Transport System ASCMinor Histocompatibility AntigensSLC1A5 protein, humanhepatocellular carcinomaM2 macrophagespan-cancerproliferationSLC1A5

Identifiers

PMID40031971
PMCPMC11875851

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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.