ArticleWorld journal of surgical oncology2025
IGF2BP1 promotes the progression of head and neck squamous cell carcinoma by activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition.
Article in World journal of surgical oncology, 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
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
1 citing paper in PubMed.
- The Oncogenic Role of Long Non-Coding RNABiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundHead and neck squamous cell carcinoma (HNSCC) ranks as the sixth most prevalent cancer globally, with lymph node metastasis being a primary contributor to poor patient prognosis. Elucidating the molecular mechanisms driving HNSCC lymphatic metastasis is imperative for developing targeted therapeutic strategies and improving patient survival.
methodsThe expression of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in HNSCC samples was evaluated using The Cancer Genome Atlas (TCGA), RT-qPCR, Western blotting, and immunohistochemical analysis. The impact of IGF2BP1 on HNSCC cell proliferation was assessed through CCK-8 assay, plate cloning, and EdU assays. Cell motility was examined by Transwell migration and invasion assays. A tumor lymph node metastasis model in nude mice was established to evaluate the role of IGF2BP1 in lymphatic metastasis. Additionally, the regulatory effects of IGF2BP1 on the epithelial-mesenchymal transition (EMT) and the PI3K/AKT/mTOR signaling pathways were investigated using immunofluorescence and Western blotting.
resultsIGF2BP1 expression was significantly elevated in HNSCC tissues compared to adjacent normal tissues and was strongly associated with lymph node metastasis and poor prognosis. Knockdown of IGF2BP1 suppressed the proliferation, migration, and invasion of HNSCC cells. Furthermore, IGF2BP1 knockdown inhibited tumor growth and lymphatic metastasis in vivo. Mechanistically, IGF2BP1 was found to promote the EMT process by activating the PI3K/AKT/mTOR pathway, thereby enhancing the migratory and invasive capabilities of HNSCC cells.
conclusionsOur findings demonstrate that IGF2BP1 plays a critical role in promoting HNSCC growth and metastasis, highlighting its potential as a therapeutic target.
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.