ArticleInternational journal of biological sciences2025
N
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- PDIA1 promotes androgen receptor activation and prostate cancer cell survival through enhancing HMMR stability.FEBS letters · 2026Article
- RNA-binding protein hnRNPD induces epithelial-mesenchymal transition in Wilms' tumor via facilitating MAP4K4 mRNA stability.Molecular genetics and genomics : MGG · 2026Article
- IGF2BP2 Promotes Oral Squamous Cell Carcinoma Progression and Is Associated with MAPK Signaling and Macrophage-Related Immune Features.ACS omega · 2026Article
- HMMR in human cancers: regulatory mechanism and biological function.Journal of translational medicine · 2025Review
- The mMolecular biomedicine · 2025Review
- PSMD14 drives lung adenocarcinoma progression through HMMR stabilization and dual activation of TGF-β/Smad and PI3K/AKT/mTOR signaling.Frontiers in immunology · 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Globally, lung cancer represents the leading cause of cancer-related mortality, with 85% of cases attributable to non-small cell lung cancer (NSCLC). Metastatic progression remains a major challenge in treating advanced lung cancer, resulting in a dismal five-year survival rate of 20-30%. Hyaluronan mediated motility receptor (HMMR) has been identified as a novel oncogene in NSCLC. However, its exact role and mechanisms in NSCLC and metastasis are yet to be fully understood. Elevated mRNA and protein levels of HMMR were observed in human NSCLC tumors in comparison with normal adjacent tissues. Increased HMMR expression was associated with poorer prognosis, with multivariate Cox regression analysis also identifying it as an independent prognostic factor. HMMR knockdown inhibited tumor cell migration and invasion, while its overexpression enhanced these processes. Mechanistically, HMMR promotes tumor metastasis by binding to mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4), which activates the p-JNK/p-c-JUN/MMP1 signaling cascade. The effects of HMMR overexpression on metastatic potential and JNK signaling were confirmed by MAP4K4 knockdown or GNE-495 treatment. Additionally, insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) was found to bind to the N
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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 OpenQuestion graph.