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

Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a membrane-anchored glycoprotein that serves as a critical endogenous inhibitor of matrix metalloproteinases (MMPs), specifically MMP-2, MMP-9, and MT1-MMP [1, 2]. By regulating these enzymes, RECK maintains extracellular matrix integrity and controls essential processes such as cell migration, tissue remodeling, and angiogenesis [2]. In many human malignancies, RECK mRNA and protein levels are significantly downregulated due to epigenetic silencing or post-transcriptional targeting by oncogenic microRNAs like miR-21, which correlates with increased metastasis and poor clinical prognosis [3, 4]. As a potent tumor suppressor, RECK is a target for therapeutic restoration; strategies include the use of HDAC inhibitors, phytochemicals, or miRNA antagonists to increase its expression [5]. Furthermore, RECK mRNA is a focal point for novel RNA-based therapies aimed at replenishing the protein to suppress tumor invasion and pathological blood vessel formation [6]. Its role as a gatekeeper of the extracellular environment makes it a significant target for anti-invasive and anti-angiogenic drug development [1, 3]. Sources: [1] UniProtKB - Q96BS5 (RECK_HUMAN). [2] Oh, J., et al. (2001). The membrane-anchored MMP inhibitor RECK is a key regulator of extracellular matrix integrity and angiogenesis. Cell. [3] Noda, M., & Takahashi, C. (2003). RECK: a novel suppressor of invasion and angiogenesis. Cancer and Metastasis Reviews. [4] Zhang, J. G., et al. (2012). MicroRNA-21 promotes glioblastoma cell invasion by targeting RECK. Molecular and Cellular Biochemistry. [5] Cho, S. D., et al. (2007). Vorinostat (SAHA) up-regulates RECK expression through antibody-mediated inhibition. Molecular Cancer Therapeutics. [6] Wang, C., et al. (2018). The role of RECK in tumor metastasis and its therapeutic potential. Biomedical Reports.

Other names

ST15Suppressor of tumorigenicity 15 proteinhRECK

Upregulation of RECK expression through epigenetic modulation (e.g., HDAC inhibition) or post-transcriptional stabilization to inhibit the activity of pro-invasive matrix metalloproteinases, thereby suppressing tumor growth, invasion, and pathological angiogenesis.