RETRACTED ARTICLE: The Clinical Utility of Matrix Metalloproteinase 9 in Evaluating Pathological Grade and Prognosis of Glioma Patients: A Meta-Analysis

Yang, Xijia; Lv, Shunzeng; Liu, Yuting; Li, Daotang; Shi, Ranran; Tang, Zhenyu; Fan, Jianzhen; Xu, Zuo-Feng

doi:10.1007/s12035-014-8850-2

Cited by 24 publications

(8 citation statements)

References 16 publications

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“…Yang et al . () performed a meta‐analysis of studies on MMP‐9 in glioma and concluded that MMP‐9 is highly associated with high‐grade glioma and a poor 5‐year prognosis and that MMP‐9 testing in glioma tissues should be a routine clinical protocol in pathology departments.…”

Section: Pathologies: Predisposition Diagnosis and Therapy (Animal mentioning

confidence: 99%

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Vafadari

Salamian

Kaczmarek

2016

Journal of Neurochemistry

311

257

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Matrix metalloproteinase-9 (MMP-9) is a member of the metzincin family of mostly extracellularly operating proteases. Despite the fact that all of these enzymes might be target promiscuous, with largely overlapping catalogs of potential substrates, MMP-9 has recently emerged as a major and apparently unique player in brain physiology and pathology. The specificity of MMP-9 may arise from its very local and time-restricted actions, even when released in the brain from cells of various types, including neurons, glia, and leukocytes. In fact, the quantity of MMP-9 is very low in the naive brain, but it is markedly activated at the levels of enzymatic activity, protein abundance, and gene expression following various physiological stimuli and pathological insults. Neuronal MMP-9 participates in synaptic plasticity by controlling the shape of dendritic spines and function of excitatory synapses, thus playing a pivotal role in learning, memory, and cortical plasticity. When improperly unleashed, MMP-9 contributes to a large variety of brain disorders, including epilepsy, schizophrenia, autism spectrum disorder, brain injury, stroke, neurodegeneration, pain, brain tumors, etc. The foremost mechanism of action of MMP-9 in brain disorders appears to be its involvement in immune/inflammation responses that are related to the enzyme's ability to process and activate various cytokines and chemokines, as well as its contribution to bloodbrain barrier disruption, facilitating the extravasation of leukocytes into brain parenchyma. However, another emerging possibility (i.e., the control of MMP-9 over synaptic plasticity) should not be neglected. The translational potential of MMP-9 has already been recognized in both the diagnosis and treatment domains. The most striking translational aspect may be the discovery of MMP-9 up-regulation in a mouse model of Fragile X syndrome, quickly followed by human studies and promising clinical trials that have sought to inhibit MMP-9. With regard to diagnosis, suggestions have been made to use MMP-9 alone or combined with tissue inhibitor of matrix metalloproteinase-1 or brain-derived neurotrophic factor as disease biomarkers.

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Section: Pathologies: Predisposition Diagnosis and Therapy (Animal mentioning

confidence: 99%

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Vafadari

Salamian

Kaczmarek

2016

Journal of Neurochemistry

311

257

View full text Add to dashboard Cite

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“…PCNA, the expression of which is elevated in proliferating cells and in most malignant tumor cells, is commonly used as a proliferative/malignancy biomarker in cancer [25]. In addition, expression of MMP-9, which is associated with cell migration and extracellular matrix degradation, reflects the migration and invasion of tumor cells [26]. Our data suggest that SDC1 knockdown inhibits the proliferation and invasion of A172 and U87 cells by inhibiting PCNA and MMP-9 expression.…”

Section: Discussionmentioning

confidence: 99%

Syndecan-1 knockdown inhibits glioma cell proliferation and invasion by deregulating a c-src/FAK-associated signaling pathway

et al. 2017

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Recent studies have shown that increased syndecan-1 (SDC1) expression in human glioma is associated with higher tumor grades and poor prognoses, but its oncogenic functions and the underlying molecular mechanisms remain unknown. Here, we examined SDC1 expression in datasets from The Cancer Genome Atlas and the National Center for Biotechnology Information Gene Expression Omnibus. Elevated SDC1 expression in glioma was closely associated with increases in tumor progression and shorter survival. We also examined SDC1 expression and evaluated the effects of stable SDC1 knockdown in glioma cell lines. SDC1 knockdown attenuated proliferation and invasion by glioma cells and markedly decreased PCNA and MMP-9 mRNA and protein expression. In a xenograft model, SDC1 knockdown suppressed the tumorigenic effects of U87 cells in vivo. SDC1 knockdown decreased phosphorylation of the c-Src/FAK complex and its downstream signaling molecules, Erk, Akt and p38 MAPK. These results suggest that SDC1 may be a novel therapeutic target in the treatment of glioma.

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“…Gliomas have been reported as the most common one of primary cerebral tumors in central neural system. According to the regulation of World Health Organization (WHO) classification stantard, all gliomas can be divided into 4 grades on the basis of their histology [1][2]. Although some latest therapy technologies (resection and radio-/chemotherapy) have been introduced into the treatment of gliomas, the whole effects on patients with gliomas remain to be not satisfactory [3][4].…”

Section: Introductionmentioning

confidence: 99%

MiR-26b suppresses cell proliferation and invasion by targeting cyclooxygenase 2 in human glioblastoma

Jiang¹,

Liu²,

Zhang³

et al. 2016

Oncotarget

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MiRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers. Aberrant miRNA expression has been observed in human glioblastoma (GBM). The present study was to evaluate the expression and molecular mechanisms of COX-2 and miR-26b in human GBM tissues and GBM cell lines T98G, U87 and U251. In the present study, we found that expression of miR-26b was markedly downregulated in GBM cell lines and human GBM tissues, compared to matched non-tumor associated tissues. Furthermore, miR-26b expression was inversely proportional to that of COX-2 mRNA and protein. Ectopic expression of miR-26b dramatically reduced the proliferation, colony formation, and proliferation/apoptosis-related proteins in GBM cells. Flow cytometry analysis showed that ectopic expression of miR-26b significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Finally, luciferase reporter assay revealed that miR-26b inhibited the expression of COX-2 by binding to the 3'-UTR of COX-2 in GBM cells. Taken together, our results suggest that miR-26b plays an important role to inhibit the proliferation and invasion of GBM cells, and presents a novel mechanism for direct miR-26bmediated suppression of COX-2 in GBM. Thus, miR-26b/COX-2 may have an important role in treatment of GBM patients.

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RETRACTED ARTICLE: The Clinical Utility of Matrix Metalloproteinase 9 in Evaluating Pathological Grade and Prognosis of Glioma Patients: A Meta-Analysis

Cited by 24 publications

References 16 publications

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Syndecan-1 knockdown inhibits glioma cell proliferation and invasion by deregulating a c-src/FAK-associated signaling pathway

MiR-26b suppresses cell proliferation and invasion by targeting cyclooxygenase 2 in human glioblastoma

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