ADAM19: biological characteristics and implications in disease pathology and clinical applications.

Authors

Yichun Hu, Xuehan Wang, Yang Qu, Deyuan Li, Shujin Li, Dejun Hu, Hanmeng Liu, Yongkang Wu

Published in

Inflammation research : official journal of the European Histamine Research Society ... [et al.]. Volume 75. Issue 1. Sep 27, 2026. Epub Sep 27, 2026.

Abstract

This article critically examines ADAM19-mediated inflammatory remodeling within five distinct subtypes of solid tumors prone to inflammation, employing non-neoplastic inflammatory states strictly as a comparative reference. As a transmembrane protease belonging to the ADAM family, ADAM19 undergoes maturation through plasmin-dependent cleavage, with its expression tightly regulated by both transcriptional and epigenetic controls. Although dysregulated ADAM19 levels are evident in various inflammatory lesions and malignancies, its context-specific dual biological roles necessitate a systematic synthesis.
ADAM19 modulates signal transduction pathways by processing pro-inflammatory cytokines. While it generally expedites progression in the majority of solid tumors, it paradoxically suppresses tumor growth in prostate cancer and specific osteosarcoma subsets; this functional dichotomy is orchestrated by intricate non-coding RNA networks and interconnected signaling cascades. Preclinical evidence indicates that ADAM19 holds promise as both a biomarker and a therapeutic target, yet robust clinical validation remains lacking. Consequently, this review delineates ADAM19 structural characteristics, contrasts its tissue-specific regulatory mechanisms across different malignancies, and integrates exosomal and immune-related signaling axes to reconcile contradictory research findings. We highlight pivotal translational challenges, notably tissue-dependent functional heterogeneity and the scarcity of selective ADAM19 inhibitors, while proposing targeted research directions to advance future precision oncology strategies centered on ADAM19.

PMID:
42802271
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.

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