ReviewFrontiers in immunology2025
CD147 at the crossroads of glycoprotein networks, metabolic reprogramming, and metastatic progression.
Review in Frontiers in immunology, 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD147 (also known as EMMPRIN or Basigin), a transmembrane glycoprotein of the immunoglobulin superfamily, functions as a pivotal regulator of tumor progression. It coordinates key oncogenic processes-including metabolic adaptation, chemoresistance, angiogenesis, and immune modulation-through an extensive network of protein-protein interactions. Metabolic reprogramming not only reshapes the intrinsic metabolic circuitry of tumor cells but also promotes the establishment of a pre-metastatic niche that facilitates metastatic seeding and outgrowth via dynamic metabolic crosstalk with immune and stromal components. Here, we review current evidence showing that CD147 mediates PMN formation by promoting immune evasion, metabolic adaptation, and stromal remodeling. Through the coordination with membrane-associated glycoproteins-including CD44, epidermal growth factor receptor (EGFR), integrins, CD280 (uPARAP/Endo180/MRC2), and CD276, CD147 orchestrates intracellular signaling events that drive cancer cell metabolic adaptation. These interactions contribute to metabolic reprogramming across glucose, lipid, amino acid, and mitochondrial pathways, thereby linking CD147-mediated metabolic plasticity to tumor dissemination and metastasis. By integrating insights into immune and stromal modulation within the tumor microenvironment (TME), this review highlights the multifaceted roles of CD147 and its glycoprotein interactome in shaping the metastatic niche.
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.