Evidence map›Paper›PMID 40632192›Full record

ArticleBiochemical genetics2026

miR-574-3p Regulates Smad/Snail Signaling to Promote Epithelial-Mesenchymal Transition in Nasopharyngeal Carcinoma Cells.

Ping Ai, Wei Qu, Xianbing Peng, Yi Zeng

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Article in Biochemical genetics, 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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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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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

4 authors.

Ping Ai *Department of Otolaryngology, Shiyan Renmin Hospital, Shiyan, 442000, Hubei, People's Republic of China.
Wei Qu *Department of Otolaryngology, Shiyan Renmin Hospital, Shiyan, 442000, Hubei, People's Republic of China.
Xianbing PengDepartment of Otolaryngology, Shiyan Renmin Hospital, Shiyan, 442000, Hubei, People's Republic of China.
Yi ZengDepartment of Otolaryngology, Shiyan Renmin Hospital, Shiyan, 442000, Hubei, People's Republic of China. 18872021104@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is pivotal in the progression and metastasis of nasopharyngeal carcinoma (NPC). MicroRNAs (miRNAs), particularly miR-574-3p, are emerging as critical regulators in these processes. This study examines the role of miR-574-3p in NPC and its relationship with the Smad/Snail signaling pathway. Expression levels of miR-574-3p were analyzed in six NPC tumor tissues and adjacent normal tissues using qRT-PCR. Functional assays, including overexpression and inhibition of miR-574-3p, were conducted in HNE1 cells. Dual-luciferase reporter assays validated the targeting relationship between miR-574-3p and Smad7. EMT-related molecular changes were evaluated by Western blotting and migration assays. miR-574-3p was significantly upregulated in NPC tumor tissues compared to adjacent normal tissues. Overexpression of miR-574-3p promotes proliferation and migration and inhibits apoptosis in HNE1 cells. Moreover, miR-574-3p upregulation inhibited Smad7 and Snail expression, reducing EMT markers (α-SMA and Twist1), while its inhibition had the opposite effects. Dual-luciferase assays confirmed that miR-574-3p directly targets Smad7. This study reveals that miR-574-3p inhibits the EMT process of NPC cells by regulating the Smad/Snail signaling pathway, providing a new potential therapeutic target for the treatment of NPC.

Indexed as

Epithelial-Mesenchymal TransitionMicroRNAsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsSignal TransductionSmad7 ProteinSnail Family Transcription FactorsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMicroRNAsSmad7 ProteinSMAD7 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsEpithelial-mesenchymal transitionmiR-574-3pNasopharyngeal carcinomaSmad/Snail signaling pathway

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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.