Evidence map›Paper›PMID 41776690›Full record

ArticleHereditas2026

miR-3913-3p promoted the progression of lung adenocarcinoma by regulating STX3 expression.

Yu Wang, Lin Shen, Ruijie Cao, Hao Xu, Zhong Guo, Yuxing Chen, Dan Wang

Abstract read
In one paragraph

Article in Hereditas, 2026. 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

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

Who cites it

1 citing paper in PubMed.

  1. Article
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

7 authors.

Yu WangInstitute of Upper Gastrointestinal Tumour Prevention and Treatment, Shanxi Medical University, Changzhi, 046000, China.
Lin ShenIntegrated Traditional Chinese and Western Medicine, Qingdao Central Hospital, University of Health and Rehabilitation Sciences (Qingdao Central Hospital), Qingdao, 266042, China.
Ruijie CaoDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Jinshan Branch, Shanghai, 201599, China.
Hao XuDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Jinshan Branch, Shanghai, 201599, China.
Zhong GuoDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Jinshan Branch, Shanghai, 201599, China.
Yuxing ChenDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Jinshan Branch, Shanghai, 201599, China.
Dan WangDepartment of Respiratory and Critical Care Medicine, Huanggang Central Hospital, No. 6, Qi'an Avenue, Huangzhou District, Huanggang, 438000, China. WangDan_hg@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe prognostic relevance and operational pathways of miR-3913-3p during disease advancement are not entirely clarified. This research intends to thoroughly assess the clinical importance and mechanistic contributions of miR-3913-3p within lung adenocarcinoma (LUAD) contexts.

methodsRelationships linking miR-3913-3p abundance with five-year survival rates were examined through Kaplan-Meier methodology, while prognostic strength was determined by multivariate Cox regression modeling. Quantification of miR-3913-3p and STX3 in clinical specimens and cellular models was accomplished via RT-qPCR. Functional impacts on LUAD cells and regulatory interactions with target genes were validated through cell transfection, CCK-8 assays, Transwell migration/invasion assays, and dual-luciferase reporter assays.

resultsmiR-3913-3p expression was significantly elevated in LUAD tissues compared to matched non-tumor tissues. High miR-3913-3p expression was significantly correlated with poor tumor differentiation, advanced TNM stage, and lymph node metastasis (p < 0.05). Multivariate Cox analysis identified high miR-3913-3p expression as a predictor of poor prognosis (HR = 2.450, 95% CI: 1.014–5.920, p = 0.046). Functionally, miR-3913-3p mimic enhanced the proliferative, migratory, and invasive capacities of LUAD cells, whereas miR-3913-3p inhibitor suppressed these malignant behaviors. Notably, co-transfection with si-STX3 rescued the inhibitory effects induced by the miR-3913-3p inhibitor. Mechanistically, dual-luciferase reporter assays confirmed that miR-3913-3p directly binds to the 3’untranslated region (3’UTR) of STX3, leading to its functional suppression.

conclusionThis study demonstrates the existence of a regulatory miR-3913-3p/STX3 axis in LUAD. miR-3913-3p likely promotes the proliferation, migration, and invasion of LUAD cells by targeting STX3, implicating this axis in LUAD pathogenesis.

Indexed as

Adenocarcinoma of LungGene Expression Regulation, NeoplasticLung NeoplasmsMicroRNAsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleHumansMaleMiddle AgedPrognosisMicroRNAsInvasionLUADMigrationmiR-3913-3pProliferationSTX3

Identifiers

PMID41776690
PMCPMC13067435

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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.