Evidence map›Paper›PMID 42432839›Full record

ArticleJournal of cellular and molecular medicine2026

TFAP2A-Induced Upregulation of LncRNA NUTM2A-AS1 Promotes LUAD Progression Through a miR-409-5p/SLC35F2 Regulatory Axis.

Weiqin Wang, Yongfeng Liu, Tiantian Chen, Jing Zhang, Feng Hu

Abstract read
In one paragraph

Article in Journal of cellular and molecular 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.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Weiqin WangDepartment of Respiratory and Critical Care Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yongfeng LiuDepartment of Respiratory and Critical Care Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tiantian ChenDepartment of Respiratory and Critical Care Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jing ZhangDepartment of Respiratory and Critical Care Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Feng HuDepartment of Respiratory and Critical Care Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0007-4533-7677

Funding

Shanghai Changning District Committee of Science and Technology CNKW2022Y05
6 · The paper itself

Abstract

Long non-coding RNAs (LncRNAs) play pivotal roles in lung adenocarcinoma (LUAD) progression. However, the upstream transcriptional regulation and downstream mechanisms of LncRNA NUTM2A-AS1 in LUAD remain largely unexplored. The expression levels of NUTM2A-AS1, TFAP2A, miR-409-5p and SLC35F2 in LUAD tissues and cell lines were analysed using public databases and qRT-PCR. The biological functions of this axis in LUAD cells were evaluated through CCK-8, Transwell and apoptosis assays. The molecular interactions among TFAP2A, NUTM2A-AS1, miR-409-5p and SLC35F2 were validated via chromatin immunoprecipitation (ChIP), dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Both NUTM2A-AS1 and TFAP2A were significantly upregulated in LUAD and correlated with poor prognosis. Mechanistically, the transcription factor TFAP2A directly bound to the NUTM2A-AS1 promoter to activate its transcription. Functionally, NUTM2A-AS1 promoted LUAD cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), while suppressing apoptosis. Furthermore, NUTM2A-AS1 may function as a competing endogenous RNA-like regulator by interacting with miR-409-5p, thereby upregulating the expression of the solute carrier family member SLC35F2. Rescue assays demonstrated that SLC35F2 knockdown attenuated the oncogenic phenotypes induced by TFAP2A or NUTM2A-AS1, while miR-409-5p restoration suppressed SLC35F2 expression and cell-cycle progression. Our study supports a TFAP2A/NUTM2A-AS1/miR-409-5p/SLC35F2 regulatory model that contributes to LUAD progression. These findings suggest that the TFAP2A/NUTM2A-AS1/miR-409-5p/SLC35F2 axis contributes to LUAD progression and may provide potential biomarkers and therapeutic targets.

Indexed as

Adenocarcinoma of LungGene Expression Regulation, NeoplasticLung NeoplasmsMicroRNAsRNA, Long NoncodingTranscription Factor AP-2Up-RegulationApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionHumansMicroRNAsRNA, Long NoncodingTFAP2A protein, humanTranscription Factor AP-2LncRNAlung adenocarcinomamiRNASLC35F2TFAP2A

Identifiers

PMID42432839
PMCPMC13354745

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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.