ArticleCanadian respiratory journal2025
LINC01214 Promotes Non-Small Cell Lung Cancer Through the miR-497-3p/HSP90AB1 Axis.
Article in Canadian respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The lncRNA OTX2-AS1 promotes NSCLC progression via the miR-377-5p/EIF5A2 axis and EMT induction.World journal of surgical oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aimed to explore the potential of LINC01214 in providing prognostic and therapeutic insights, thereby offering valuable references for the research of non-small cell lung cancer (NSCLC). Methods: 122 NSCLC subjects were recruited. The molecular level was quantified by qPCR and WB. Kaplan-Meier estimated the prognostic effects and Cox regression analyses the hazard ratio. The cell activities including proliferation, apoptosis, and migration/invasion were evaluated by CCK-8, flow cytometry, and Transwell. The regulatory axis of LINC01214/miR-497-3p/HSP90AB1 was verified by the dual luciferase reporter assay and rescue experiments. Results: LINC01214 increased both in the malignant tissues and cell lines of NSCLC. Mortality was increased in NSCLC patients with high LINC01214 levels. LINC01214 was an independent risk predictor of prognosis in NSCLC. Silencing of LINC01214 inhibited the NSCLC cell proliferation, migration, and invasion and promoted apoptosis. The abundance of miR-497-3p showed an opposite trend to LINC01214. LINC01214 could target miR-497-3p and negatively correlate with miR-497-3p. The inhibitory effect of LINC01214 on cell activity was reversed by miR-497-3p. HSP90AB1 was predicted and further confirmed as the target of miR-497-3p. The LINC01214/miR-497-3p/HSP90AB1 axis regulated NSCLC cell proliferation, migration, and invasion. Conclusion: LINC01214, a potential biomarker, contributed to the progression of NSCLC through the miR-497-3p/HSP90AB1 axis by promoting cell proliferation and motility.
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Registered trials
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