Reversion-inducing cysteine-rich protein with Kazal motifs (RECK)

Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a glycosylphosphatidylinositol (GPI)-anchored membrane-bound regulatory protein essential for embryogenesis, extracellular matrix (ECM) homeostasis, and tumor suppression[1][3]. RECK exerts its function primarily by negatively regulating the activity or expression of matrix metalloproteinases (MMPs), ADAMs, and ADAMTSs, which play pivotal roles in ECM remodeling, cell migration, invasion, and inflammatory processes[1][3]. RECK is broadly expressed in normal tissues and is frequently downregulated in various cancers, where its loss is associated with enhanced metastasis and poor prognosis[1][3]. Restoration of RECK expression can reverse metastatic phenotypes in cancer models[1][3]. RECK is also implicated in cardiovascular and fibrotic diseases and participates in key developmental signaling pathways such as Notch and Wnt[4][5]. Despite previous suggestions that RECK directly inhibits the enzymatic activity of MMPs, more recent studies indicate its effects may be mediated through non-catalytic regulatory mechanisms[3]. As a tumor and fibrosis suppressor, RECK is under consideration as a potential therapeutic target and biomarker in cancer and fibrotic diseases[1][3].

Other names

RECKReck proteinGPI-anchored metalloproteinase regulator

Negative regulation of MMP (and ADAM, ADAMTS) expression/activation, Inhibition of extracellular matrix degradation, Modulation of signaling pathways (Notch, Wnt, IL-6/EGFR transactivation)