ArticleThoracic cancer2025
Sortilin-1, Targeted by miR-146a, Regulates the Behavior of Non-Small Cell Lung Cancer.
Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Decoding miRNA‑146a: Mechanisms of action in cardiovascular diseases and endocrine metabolic disorders (Review).International journal of molecular medicine · 2026Review
- Sortilin-1, Targeted by miR-146a, Regulates the Behavior of Non-Small Cell Lung Cancer.Thoracic cancer · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundSortilin-1 (SORT1) has been implicated in the pathogenesis of various malignancies, but its role in non-small cell lung cancer (NSCLC) remains to be elucidated.
methodsImmunohistochemistry was employed to assess the expression of SORT1 in cancerous tissues compared to adjacent non-cancerous tissues. NSCLC cell lines, including A549, H1299, and PC-9, underwent treatment with miR-146a mimics or SORT1 small interfering RNA (siRNA), followed by evaluations of cell viability, migration, invasion, and apoptosis using cell counting kit-8, transwell assays, and scratch wound assays. Additionally, bioinformatic methods were employed to predict miR-146a target genes, which were subsequently validated through dual-luciferase reporter assays.
resultsSORT1 was significantly elevated in NSCLC tissues compared to adjacent non-cancerous counterparts. Downregulation of SORT1 inhibited proliferation, invasion, migration of tumor cell lines and promoted apoptosis. Moreover, SORT1 was a direct target of miR-146a. MiR-146a modulated tumor cell proliferation, migration, invasion, and apoptosis by suppressing SORT1 expression.
conclusionThese results suggest that miR-146a plays a critical role in the pathogenesis of NSCLC by targeting SORT1, highlighting its potential as a therapeutic target for NSCLC.
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Registered trials
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 Socratic graph.