ArticleJournal of thoracic disease2025
NUF2 promotes the malignant development of lung adenocarcinoma through the mTORC1 signaling pathway via binding to BUB1B.
Article in Journal of thoracic disease, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung adenocarcinoma (LUAD), the most prevalent subtype of non-small cell lung cancer (NSCLC), remains a leading cause of cancer-related mortality globally. Despite advances in therapy, treatment resistance and poor prognosis necessitate novel therapeutic targets. Nuclear filament-containing protein 2 (NUF2), a component of the nuclear division cycle 80 (NDC80) complex, is implicated in oncogenesis, but its role and molecular mechanisms in LUAD are poorly understood. The aim of this study is to explore the role of NUF2 in malignant development of LUAD Methods: Bioinformatics analysis using Gene Expression Profiling Interactive Analysis (GEPIA) and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) databases evaluated NUF2/BUB1B (BUB1 mitotic checkpoint serine/threonine kinase B) expression and interactions. Functional assays (cell counting kit-8, colony formation, apoptosis, wound healing, transwell) and molecular techniques (real-time quantitative polymerase chain reaction, Western blot, co-immunoprecipitation) were performed in LUAD cell lines (A549, PC-9, NCI-H1975). The binding of NUF2 and BUB1B was verified by co-immunoprecipitation assay. An Results: NUF2 was significantly upregulated in LUAD tissues and correlated with advanced stage and poor survival (P<0.001). Silencing NUF2 suppressed proliferation, migration, and invasion while promoting apoptosis in A549 cells. Mechanistically, NUF2 directly bound to BUB1B, a mitotic checkpoint kinase, and regulated the mTORC1 pathway. Overexpression of BUB1B rescued the anti-tumor effects of NUF2 knockdown, restoring mTORC1 activity (evidenced by phosphorylation of 4EBP1 and S6). Conclusions: NUF2 drives LUAD progression via BUB1B-mediated mTORC1 activation. Targeting the NUF2/BUB1B axis may offer a promising therapeutic strategy to mitigate LUAD malignancy. These findings provide critical insights into the molecular underpinnings of LUAD and highlight potential pathways for clinical intervention.
Indexed as
Identifiers
What 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.