ArticleBMC cancer2026
NT5E promotes colorectal cancer progression and correlates with PD-L1 expression: evidence from multi-omics analysis, clinical samples, and cellular functional assays.
Article in BMC cancer, 2026. 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
5 authors.
Funding
Abstract
backgroundExtracellular 5'-nucleotidase (NT5E/CD73) plays a pivotal role in the tumor immune microenvironment by catalysing the production of adenosine. This study aims to evaluate the expression and function of NT5E in colorectal cancer progression, and to explore its potential as a novel biomarker and for associated immunotherapy.
methodsGenomic alterations, prognostic significance, and immune landscape of NT5E were analyzed using cBioPortal, Kaplan‑Meier Plotter, the cancer genome atlas(TCGA)and the Human Protein Atlas. Following siRNA‑mediated knockdown in HCT116 cells, proliferation, migration, and invasion were assessed. NT5E and PD‑L1 expression were examined in 40 paired colorectal cancer specimens by qRT‑PCR. The regulatory relationship between PD‑L1 and NT5E was further validated in vitro.
resultsNT5E alterations were identified in 5.17% of CRC patients, primarily manifested as high mRNA expression and amplification. Elevated NT5E expression was significantly correlated with poorer overall survival and relapse‑free survival, particularly in patients with advanced stage, CMS1 (Consensus Molecular Subtypes 1), CMS4, and high microsatellite instability (MSI-H) subtypes. Gene set enrichment analysis revealed enrichment of purine metabolism, sphingolipid signaling, focal adhesion, and T cell receptor signaling pathways in NT5E‑high tumors. NT5E expression was positively correlated with helper T cells, macrophages, and mast cells, while negatively correlated with NK CD56dim cells. A significant positive correlation was observed between NT5E and PD‑L1, HAVCR2, and TIGIT. In clinical specimens, NT5E was upregulated in 65% of colorectal cancer tissues and positively associated with lymph node metastasis and PD‑L1 expression. In vitro experiments demonstrated that NT5E knockdown suppressed the proliferation, migration, and invasion of colorectal cancer cells, and confirmed that PD‑L1 regulates NT5E expression in colon cancer cells.
conclusionNT5E accelerates disease progression by promoting malignant biological behaviors in colorectal cancer and synergistically shaping an immunosuppressive microenvironment with PD-L1. Its overexpression constitutes an independent adverse prognostic factor. This discovery offers novel insights for anti-PD-1/PD-L1 combination immunotherapy.
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.