ArticleCell biochemistry and biophysics2025
Long Noncoding RNA NKX2-1-AS1 Accelerates Non-Small Cell Lung Cancer Progression through the miR-589-5p/NME1 Axis.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is the most common malignancy worldwide, with a high death rate. Long noncoding RNA (LncRNA) NKX2-1 antisense RNA 1 (NKX2-1-AS1) has been reported to be an oncogene in lung tumorigenesis. However, the precise mechanism of NKX2-1-AS1 underlying NSCLC progression is blurry. The intention of our research was to probe the potential mechanism of NKX2-1-AS1 underlying NSCLC. NKX2-1-AS1 expression and relevant downstream gene expression were measured using RT-qPCR. Cell proliferation and apoptosis were determined by MTT assay, EdU assay along with flow cytometry analysis. Cell migratory and invasive abilities were inspected by transwell assay. Western blot and immunofluorescence staining were utilized to assess the levels of epithelial-mesenchymal transition (EMT)-related proteins. RNA pull-down together with luciferase reporter assays were performed to verify the interaction between NKX2-1-AS1 and its downstream RNAs. Xenograft tumor-bearing mouse models were built to analyze tumor growth in vivo. The results suggested that NKX2-1-AS1 was upregulated in NSCLC patient tissues and cell lines. NKX2-1-AS1 deficiency suppressed cell proliferation, migration, invasion and EMT while elevated apoptosis. NKX2-1-AS1 bound to miR-589-5p, and NME/NM23 nucleoside diphosphate kinase 1 (NME1) was targeted by miR-589-5p in NSCLC cells. Additionally, NKX2-1-AS1 accelerated the progression of NSCLC by regulating miR-589-5p/NME1 axis. NKX2-1-AS1 knockdown repressed tumor growth in vivo. In conclusion, NKX2-1-AS1 accelerated the NSCLC progression through interacting with miR-589-5p for NME1 upregulation, which may provide clues for NSCLC targeting therapy.
Indexed as
Identifiers
39117986What OpenQuestion holds
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 OpenQuestion graph.