ArticleJournal of translational medicine2026
NGF-mediated tumor-stroma crosstalk promotes prostate cancer aggressiveness.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Stromal Regulation of Tumor Perineural Invasion: A Multicellular and Neuro-Ecological Perspective.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 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
5 authors.
Funding
Abstract
backgroundNerve growth factor (NGF) is involved in prostate cancer (PC) pathogenesis and progression. Nevertheless, its source and its role in tumor microenvironment remain still unclear as well as its contribution to tumor–stroma interactions.
methodsSingle-cell transcriptomics analysis from multiple PC datasets was performed to identify the NGF-expressing cell populations. Primary cancer-associated fibroblasts (CAFs) isolated from PC patient’s specimens were analyzed for NGF secretion and expression of the NGF receptor, TrkA. 3D tumor-stroma co-cultures were used to investigate the NGF-mediated interactions between CAFs and epithelial PC cells. Migration, invasion, and perineural invasion (PNI) assays were done to evaluate the functional outcomes, alongside the pharmacological and antibody-based inhibition of NGF/TrkA axis.
resultsHigh NGF expression correlates with reduced disease-free survival in PC patients. Single-cell analyses reveal that stromal fibroblasts and myofibroblasts are the main sources of NGF within the PC microenvironment. Primary CAFs secrete NGF and express TrkA, supporting the existence of an autocrine signaling loop. In 3D co-cultures, NGF promotes CAF spatial organization around tumor spheroids, increases spheroid size, and induces EMT-like changes in epithelial PC cells. CAF-derived NGF further stimulates directional migration and invasion in both, CAFs and tumor cells. Blockade of NGF by neutralizing antibodies or pharmacological TrkA inhibition impairs such effects. In a PNI-like assay, CAF-derived NGF facilitates tumor cell migration across neuronal layers, underscoring its role in perineural invasion.
conclusionsThe present findings identify fibroblasts as the major source of NGF within the PC microenvironment, demonstrating the existence of a reciprocal NGF–TrkA signaling loop between CAFs and PC-derived cells. This axis promotes tumor growth, epithelial plasticity, and perineural invasion, identifying NGF as a key mediator of tumor–stroma crosstalk and a potential therapeutic target in prostate cancer.
Indexed as
Identifiers
What Socratic 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 Socratic graph.