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High MMP14 and low decorin expression correlate with disease progression and metastasis in Brazilian prostate cancer patients

Amanda L. Francelino; Fernando Terzioti; Glauco A. F. Vitiello; Phelipe Oliveira Favaron; André L. L. Vanzela; Alda F. M. L. Guembarovski; Carlos A. Miqueloto; Karen B. de Oliveira; Roberta L. Guembarovski
Journal of Molecular Histology · Vol. 57, Issue 4 · 2026

Abstract

Prostate cancer (PCa) remains a highly prevalent malignancy and a leading cause of cancer-related mortality, frequently attributed to late-stage diagnosis. Matrix metalloproteinase 14 (MMP14) and Decorin (DCN) are key extracellular matrix (ECM) components essential for tissue remodeling and tumor suppression. This study evaluated the immunohistochemical expression of MMP14 and DCN in relation to clinicopathological parameters in PCa tissue samples ( n = 92), specifically examining the malignant epithelium, adjacent non-tumor tissue, and peritumoral stroma. High MMP14 expression in tumor cells was predominant in metastatic patients and significantly associated with the presence of metastases ( p = 0.012), with overexpression observed in 60% of these cases. Conversely, diminished DCN staining in the peritumoral ECM was linked to metastatic disease (63% low expression). Furthermore, a significant correlation was identified between low stromal DCN expression and ISUP grades 4–5 ( p = 0.047; 66% of high-grade cases). Multivariate analysis confirmed that MMP14 expression profile serves as an independent predictor of metastasis ( p = 0.01). In conclusion, our findings suggest that ECM remodeling, driven by dysregulation of MMP14 and DCN, plays a pivotal role in PCa progression, highlighting their potential as prognostic biomarkers for patient stratification and therapeutic guidance.

Bibliographic Information

JournalJournal of Molecular Histology
PublisherSpringer
Publication Date2026-08-01
Publication Year2026
Volume57
Issue4
Document TypeJournal Article
Print ISSN1567-2379
eISSN1567-2387
DOI10.1007/s10735-026-10869-1

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NARA Access Coverage1968-01-01~Current
Journal Homepagehttps://www.springer.com/journal/10735
Publisher PageOpen Publisher Page
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