Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.35 (matrix metalloproteinase 9)
 2,207 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the expression of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) on peripheral blood mononuclear cells (PBMCs), the serum concentration of matrix metalloproteinase 9 (MMP-9) and the MMP-9 secretion ability of PBMCs in patients with systemic lupus erythematosus (SLE), and clinical features were assessed. Compared with PBMCs from healthy donors, PBMCs from SLE patients expressed less RECK protein and mRNA but secreted more MMP-9. The serum concentration of MMP-9 was, however, lower in SLE patients than in healthy donors. The level of RECK protein was inversely associated with the Systemic Lupus International Collaborating Clinics (SLICC) Damage Index (SDI) and MMP-9 secretion in SLE, but no relationship was found between serum MMP-9 concentration and the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). In conclusion, the level of RECK protein expressed in PBMCs could be used to predict organ or system damage in SLE and this might help in developing new therapies for SLE targeted at MMP-9.
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PMID:Expression of reversion-inducing cysteine-rich protein with Kazal motifs in peripheral blood mononuclear cells from patients with systemic lupus erythematosus: links to disease activity, damage accrual and matrix metalloproteinase 9 secretion. 1865 66

This study aimed to concurrently investigate the expressions of receptor for advanced glycation end products (RAGE), reversion inducing cysteine-rich protein with Kazal motifs (RECK) and matrix metalloproteinase 9 (MMP9) in nasopharyngeal carcinoma (NPC) and their correlations with clinicopathological properties. Using immunohistochemistry, we found that RECK expression was downregulated in NPC tissues compared with chronic nasopharyngitis (CNT) tissues, while RAGE and MMP9 expressions were upregulated. We further found that RECK expression level was inversely correlated with MMP9 expression level in NPC, whereas RAGE expression level was positively correlated with MMP9 expression level. Moreover, aberrant expressions of these proteins had a positive correlation with the titers of EBVCA-IgA, lymphatic metastasis, recurrence and survival. Together, these findings suggest that dysregulations of RECK and RAGE expressions may be collectively involved in tumor progression of NPC by regulating MMP9 expression and that they may be a good prognostic predictors for NPC.
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PMID:Concurrent alterations of RAGE, RECK, and MMP9 protein expression are relevant to Epstein-Barr virus infection, metastasis, and survival in nasopharyngeal carcinoma. 2503 45

Breast cancer is an important and common tumour among women worldwide. We previously showed that 27-hydroxycholesterol (27HC) promoted the invasion and migration of breast cancer cells and activated signal transducer and activator of transcription 3 (STAT-3) signalling through reactive oxygen species (ROS). However, the regulation of STAT-3 signalling by ROS needs to be further explored. Here, we showed that 27HC caused the accumulation of cellular ROS, which upregulated matrix metalloproteinase 9 (MMP9) and increased the invasive ability of MCF7 and T47D cells. 27HC decreased the protein and mRNA levels of reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) in a time- and dose-dependent manner in MCF7 and T47D cells. RECK downregulation was mediated by 27HC-induced DNA methylation via ROS in MCF7 cells. RECK knockdown increased the activity and mRNA levels of MMP9, and promoted the invasion of MCF7 cells. We also found RECK knockdown upregulated the level of p-STAT-3 in MCF7 cells. Furthermore, overexpression of RECK attenuated 27HC-induced invasion in MCF7 cells. RECK overexpression also inhibited p-STAT-3 upregulation induced by 27HC. Collectively, the results showed that DNA methylation induced by 27HC via ROS downregulated RECK, thereby activating the STAT-3 signalling pathway. RECK could serve as a novel target mediating the effect of 27HC on breast cancer.
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PMID:Activation of STAT-3 signalling by RECK downregulation via ROS is involved in the 27-hydroxycholesterol-induced invasion in breast cancer cells. 3193 92