Single nucleotide polymorphisms of matrix metallopeptidase 3 and risk of gliomas in a Chinese Han population

Fan, Weiwei; Zhou, Keke; Hu, Dezhi; Song, Xiao; Zhao, Yingjie; Chen, Hongyan; Wei, Qingyi; Chen, Gong; Shi, Jinlong; Du, Guizhi; Mao, Ying; Lu, Daru; Zhou, Lei

doi:10.1002/mc.20842

Cited by 7 publications

(6 citation statements)

References 51 publications

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“…The current study also revealed that the protein levels of MMP-2, MMP-9, and Vimentin were increased, while the E-cadherin protein level was decreased as a result of BMP2 over-expression or activation of the MAPK/p38 signaling pathway. The MMP family represents the dominating factors in promoting central nervous system tumor growth, including invasion and spreading, and thereby is of valuable therapeutic importance [31]. In addition, it has been reported that MMP-2 activation induced by the ERK/MAPK signaling pathway contributes to the enhancement of cell proliferation and invasion in endometrial cancer [32].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: BMP2 secretion from hepatocellular carcinoma cell HepG2 enhances angiogenesis and tumor growth in endothelial cells via activation of the MAPK/p38 signaling pathway

Feng

Kuang

et al. 2019

Stem Cell Res Ther

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Background Hepatocellular carcinoma (HCC) is one of the most common tumors globally, with varying prevalence based on endemic risk factors. Bone morphogenetic protein (BMP) exhibits a broad spectrum of biological activities in various tissues including angiogenesis. Here, this study aimed to investigate the mechanism of BMP2 in HCC by mediating the mitogen-activated protein kinase (MAPK)/p38 signaling pathway. Methods BMP2 expression was quantified in HCC and adjacent tissues. BMP2 gain- and loss-of-function experiments were conducted by infection with lentivirus over-expressing BMP2 or expressing shRNA against BMP2. The angiogenesis was evaluated with HepG2 cells co-cultured with ECV304 cells. SB-239063 was applied to inhibit the activation of the MAPK/p38 signaling pathway so as to identify the significance of this pathway in HCC progression. Finally, in vivo experiments were conducted to identify the role of BMP2 and the MAPK/p38 signaling pathway in tumor growth and angiogenesis. Results BMP2 was highly expressed in HCC. Over-expression of BMP2 was found to accelerate cell proliferation, migration, invasion, microvascular density, and angiogenesis and decrease cell apoptosis in vitro and in vivo. BMP2 silencing exhibited inhibitory effects on HCC cell invasion and angiogenesis. The co-culture system illustrated that HepG2 cells secreted BMP2 in ECV304, and silenced BMP2 in HepG2 cells resulted in the inactivation of the MAPK/p38 signaling pathway, thus suppressing cancer progression, tumor growth, and angiogenesis in HCC. Conclusion Taken together, the key findings of this study propose that silencing of BMP2 inhibits angiogenesis and tumor growth in HCC, highlighting BMP2 silencing as a potential strategy for the treatment of HCC.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: BMP2 secretion from hepatocellular carcinoma cell HepG2 enhances angiogenesis and tumor growth in endothelial cells via activation of the MAPK/p38 signaling pathway

Feng

Kuang

et al. 2019

Stem Cell Res Ther

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“…Based on the results of RNA-seq, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that gene sets that were significantly differentially regulated in GMPPB knockdown cells were mainly involved in cell adhesion, axon guidance, and Hippo signaling pathways (Figure 5B). Intriguingly, we also detected MMPs (Figure 5A,D), a gene that has been previously reported to play an important role in the malignancy of glioma cells [31,[37][38][39], as one of the downstream target genes of GMPPB. Indeed, the expression of MMP3 was decreased by down-regulating GMPBB, while in GBM cells, over-expressing GMPPB increased the expression levels of MMP3 in GBM cells (Figure 5E).…”

Section: Silencing Gmppb Inhibits the Proliferation And Invasion Of G...supporting

confidence: 63%

Silencing GMPPB Inhibits the Proliferation and Invasion of GBM via Hippo/MMP3 Pathways

Huang,

Abdallah,

Shen

et al. 2023

IJMS

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Glioblastoma multiforme (GBM) is a highly aggressive malignancy and represents the most common brain tumor in adults. To better understand its biology for new and effective therapies, we examined the role of GDP-mannose pyrophosphorylase B (GMPPB), a key unit of the GDP-mannose pyrophosphorylase (GDP-MP) that catalyzes the formation of GDP-mannose. Impaired GMPPB function will reduce the amount of GDP-mannose available for O-mannosylation. Abnormal O-mannosylation of alpha dystroglycan (α-DG) has been reported to be involved in cancer metastasis and arenavirus entry. Here, we found that GMPPB is highly expressed in a panel of GBM cell lines and clinical samples and that expression of GMPPB is positively correlated with the WHO grade of gliomas. Additionally, expression of GMPPB was negatively correlated with the prognosis of GBM patients. We demonstrate that silencing GMPPB inhibits the proliferation, migration, and invasion of GBM cells both in vitro and in vivo and that overexpression of GMPPB exhibits the opposite effects. Consequently, targeting GMPPB in GBM cells results in impaired GBM tumor growth and invasion. Finally, we identify that the Hippo/MMP3 axis is essential for GMPPB-promoted GBM aggressiveness. These findings indicate that GMPPB represents a potential novel target for GBM treatment.

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“…For instance, elevated expression of MMP3 has been detected in human astrocytoma, especially in invasive glioma cells. Increased cytoplasmic MMP3 expression stimulates glioma cell invasiveness and migration [29][30][31] , making MMP3 a promising therapeutic target. The current study showed that MMP3 could be induced by GBP5 at both mRNA and protein levels in GBM cells and was essential for GBP5-driven impacts.…”

Section: Discussionmentioning

confidence: 99%

GBP5 drives malignancy of glioblastoma via the Src/ERK1/2/MMP3 pathway

Jin

Zheng

et al. 2021

Cell Death Dis

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Guanylate binding proteins (GBPs), a family of interferon-inducible large GTPase, play a pivotal role in cell-autonomous immunity and tumor malignant transformation. Glioblastoma (GBM) is the most prevalent and lethal primary brain tumor in adults. Here we show that GBP5 was highly expressed in GBM cell lines and in clinical samples, especially in the mesenchymal subtype. The expression levels of GBP5 were negatively correlated with the prognosis of GBM patients. Overexpression of GBP5 promoted the proliferation, migration, and invasion of GBM cells in vitro and in vivo. In contrast, silencing GBP5 by RNA interference exhibited the opposite effects. Consequently, targeting GBP5 in GBM cells resulted in impaired tumor growth and prolonged survival time of mice with GBM tumors. We further identified that the Src/ERK1/2/MMP3 axis was essential for GBP5-promoted GBM aggressiveness. These findings suggest that GBP5 may represent a novel target for GBM intervention.

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Single nucleotide polymorphisms of matrix metallopeptidase 3 and risk of gliomas in a Chinese Han population

Cited by 7 publications

References 51 publications

RETRACTED ARTICLE: BMP2 secretion from hepatocellular carcinoma cell HepG2 enhances angiogenesis and tumor growth in endothelial cells via activation of the MAPK/p38 signaling pathway

RETRACTED ARTICLE: BMP2 secretion from hepatocellular carcinoma cell HepG2 enhances angiogenesis and tumor growth in endothelial cells via activation of the MAPK/p38 signaling pathway

Silencing GMPPB Inhibits the Proliferation and Invasion of GBM via Hippo/MMP3 Pathways

GBP5 drives malignancy of glioblastoma via the Src/ERK1/2/MMP3 pathway

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