Evidence map›Paper›PMID 41782112›Full record

ArticleJournal of translational medicine2026

TFAP2A regulates SGPP2 transcription to promote lipid accumulation and activate the Wnt/β-catenin signaling pathway to promote malignant progression in lung adenocarcinoma.

Qingqing Li, Jiangying Li, Cui Zhang, Yuxuan Deng, Bowen Yang, Li Ma, Yuxiang Liu, Chunliang Wang, Linlin Xu, Jinhong Mei

Abstract read
In one paragraph

Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Qingqing LiDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Jiangying LiDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Cui ZhangDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Yuxuan DengDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Bowen YangDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Li MaDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Yuxiang LiuDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China.
Chunliang WangDepartment of Neurosurgery, The First affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.
Linlin XuDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China. xulinlin@ncu.edu.cn.
Jinhong MeiDepartment of Pathology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, P.R. China. ndyfy00999@ncu.edu.cn.ORCID 0009-0000-6551-4844

Funding

National Natural Science Foundation of China 82060517National Natural Science Foundation of China 82260525Natural Science Foundation of Jiangxi Province 20212ACB206015
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the leading cause of cancer-related mortality worldwide, highlighting the urgent need for additional molecular biomarkers and therapeutic targets. Transcription factor AP-2α (TFAP2A) is highly expressed in LUAD and is associated with poor prognosis. Sphingosine-1-phosphate phosphatae 2 (SGPP2/SPP2) has been implicated in tumor progression in multiple cancer types; however, its functional role in LUAD cells and the underlying mechanisms remain unclear.

methodsBioinformatics analysis was conducted to elucidate the expression patterns of SGPP2 and TFAP2A. Quantitative real-time polymerase chain reaction (qRT-PCR), western blotting (WB), and immunohistochemistry (IHC) were performed to measure mRNA and protein expression levels. Cellular proliferation and cell cycle progression were evaluated using the Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2’-deoxyuridine (EdU) assay, colony formation assay, and flow cytometry. Migratory and invasive capabilities were evaluated using transwell and wound-healing assays. Lipid metabolism was assessed by measuring triglyceride (TG) and total cholesterol (TC) levels, using Oil Red O and Nile Red fluorescence staining. The regulatory relationship between TFAP2A and the SGPP2 promoter was confirmed using chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. Protein-protein interactions were investigated using co-immunoprecipitation (CoIP) assay. The in vivo tumorigenic potential was examined using a xenograft model in nude mice.

resultsSGPP2 and TFAP2A were upregulated in LUAD. High SGPP2 expression is closely associated with lymph node metastasis. Functional experiments demonstrated that SGPP2 promotes LUAD cell proliferation, migration, and epithelial-mesenchymal transition (EMT). Under physiological conditions, TFAP2A transcriptionally activates SGPP2 in LUAD cells, whereas SGPP2 reciprocally inhibits TFAP2A expression. Downstream pathway analysis revealed that SGPP2 overexpression downregulated SGPP1 expression, leading to increased sphingosine-1-phosphate (S1P) levels in the cells. This, in turn, promotes intracellular lipid accumulation and phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser9, thereby facilitating the nuclear translocation of β-catenin. Consequently, CyclinD1 expression is upregulated, ultimately driving LUAD progression.

conclusionSGPP2 and TFAP2A are highly expressed in LUAD. SGPP2, which regulates S1P levels and is transactivated by TFAP2A, promotes lipid accumulation and activates the Wnt/β-catenin signaling pathway to facilitate the progression of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungDisease ProgressionLipid MetabolismLung NeoplasmsTranscription Factor AP-2Transcription, GeneticWnt Signaling PathwayAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleTFAP2A protein, humanTranscription Factor AP-2Lipid accumulationLung adenocarcinomaS1PSGPP2TFAP2A

Identifiers

PMID41782112
PMCPMC13067397

What OpenQuestion holds

Textmetadata
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.