Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Nanomedicine Targeting Cancer-Associated Fibroblasts in Prostate Cancer: From Biological Mechanisms to Integrated Theranostic Strategies

Qian F., Zhou J., Tang Y., Chen J., Zuo J., Gou K.

Narrative Review, published in Int J Nanomedicine (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Int J Nanomedicine (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41869404
PMCID
PMC13005641
DOI
10.2147/ijn.s588669
Citations
2

Abstract (original English)

Prostate cancer (PCa) is the second most common malignancy in men worldwide. Advanced stages are characterized by tumor heterogeneity, metastasis, and resistance to androgen deprivation therapy and chemotherapy. Cancer-associated fibroblasts (CAFs), the predominant stromal cells in the PCa tumor microenvironment (TME), critically drive tumor progression, metastasis, and therapeutic resistance. Nanomedicine represents a transformative strategy for targeting CAFs. It leverages engineered nanomaterials to achieve precise drug delivery, improved bioavailability, and multimodal theranostic capabilities, which integrate diagnosis with therapy. This review comprehensively examines advances in nanomaterial-based strategies for CAF-targeted therapy in PCa. We first delineate the biology of CAFs in PCa, encompassing their origins, activation mechanisms, key markers (e.g, α-SMA and FAP), phenotypic heterogeneity, and intricate crosstalk with cancer cells, immune cells, and the extracellular matrix (ECM). We then evaluate nanomaterial-based targeting strategies and therapeutic modalities, including CAF depletion, reprogramming, and extracellular matrix remodeling, for the treatment of PCa. Subsequently, we discuss CAF-targeted nanoplatforms for theranostics, including molecular imaging probes (e.g., 68 Ga-FAPI) and image-guided delivery systems that integrate precise diagnosis with therapy

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsHumansProstatic NeoplasmsMaleNanomedicineTumor MicroenvironmentTheranostic NanomedicineCancer-Associated Fibroblasts

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