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The authors investigated the role of MMP-2 and membrane type 1 MMP-2, an initiator of the zymogen of MMP-2, proMMP-2, and tissue inhibitors of metalloproteinases in human evolution of astrocytic tumors. ProMMP-2 and TIMP-1, but not TIMP-2, were both significantly higher in glioblastom multiforme in glioblastomas multiforme than in other grades of astrocytic tumors, according to Analyses performed using sandwich enzyme immunoassays. In addition, the expression and proMMP-2 activation ratio were notably higher in glioblastomas associated with cerebrospinal fluid dispersion in cerebrospinal fluid diffusion in glioblastomas associated with cerebrospinal fluid diffusion in glioblastomas related to cerebrospinal fluid diffusion in cerebrospinal fluid dissemination than in those not associated with CSF dissemination. ProMMP-2 and invasive growth in three-dimensional collagen gel was evident, including mock transfectants and parental cells, which led to noninvasive growth without activation. These findings show that MT1-MMP may have a role in tumor formation and CSF dissemination of glioblastoma cells in the absence of TIMP-2.
Source link: https://doi.org/10.3171/jns.2001.94.3.0464
Tetraarsenic oxide is a trivalent arsenic oxide with potent anticancer and antiangiogenic activity in several cancer cell lines at a lower dose than arsenic trioxide, which has been more commonly used in vitro and in vivo. TAO's cytotoxic concentration in malignant glioma cell lines was determined by the authors, and whether TAO would exhibit anti-invasive activity under conditions independent of cell death or apoptosis. The effect of TAO on matrix metalloproteinase secretion and membrane type 1 -MMP expression was determined using gelatin zymography and Western blot, respectively. MMP-2 and MT1-MMP expression decreased in a dose-dependent manner in all cell lines, which was in accordance with the invasion assay findings. In both cell lines, regardless of their PTEN status, the TAO reduced kinase activity of Akt on GSK-3 assay and inhibited Akt phosphorylation in a dose-dependent manner.
Source link: https://doi.org/10.3171/2014.8.jns131991
According to studies, kaempferol could reduce adhesion, migration, and invasion of MDA-MB-231 human breast carcinoma cells. The mechanism was further deciphered by kaempferol treatment, which slowed transcription factor activator protein-1 and MAPK signaling pathways. Our results also showed that kaempferol might reduce B16F10 murine melanoma cells' lung metastasis, as well as the expression of MMP-9 in vivo. These findings, combined, showed that kaempferol could prevent cancer cell migration by blocking the PKC/MAPK/AP-1 cascade and subsequent MMP-9 expression and activity. Hence, kaempferol may also serve as a therapeutic potential tumor metastasis candidate.
Source link: https://doi.org/10.1139/bcb-2014-0067
Abstract Physiology (Invadopodia), an actin-rich protrusions that mediate the extracellular matrix degradation that is required for the success of the invasive cascade, is triggered by breast cancer metastasis. In this research, we show that TC10, a p21 small GTPases subfamily of Cdc42, regulates membrane type 1 matrix metalloproteinase-driven extracellular matrix degradation at Invadopodia. For the plasma membrane surface exposure of MT1-MMP at these facilities, we show that TC10 is required.
Source link: https://doi.org/10.1038/s42003-021-02583-3
When transfected into v-Ki-transformed NIH 3T3 cells, a human fibroblast cDNA expression library was checked for cDNA clones giving rise to flat colonies. Although RECK mRNA is present in a variety of human tissues and untransformed cells, it is undetectable in tumor-derived cell lines and oncogenically transformed cells. Oncogenic signals may be related to tumor formation and metastasis, according to RECK.
Source link: https://doi.org/10.1073/pnas.95.22.13221
Gel degradation of gels was engineered starting from a characterization of the degradation kinetics of synthetic MMP substrates in the soluble form and then crosslinking into a 3D hydrogel network. Gels were used to deliver recombinant human bone morphogenetic protein-2 to the site of significant rat cranium graft tissue, which was converted into bony tissue within 4 wk at a dose of 5 g per defect.
Source link: https://doi.org/10.1073/pnas.0737381100
During prostate cancer progression in both humans and in the TRAMP mouse model, we previously reported that the calcium-binding protein S100A4 is overexpressed. We found that siRNA-mediated suppression of the S100A4 gene in significant reduced the proliferative and invasive capability of the highly invasive CaP cells PC-3. We discovered that matrix metalloproteinase 9 and its tissue inhibitor were highly responsive to S100A4 gene suppression. Cells overexpressing the S100A4 gene in a way that MMP-9 and TIMP-1 genes were also significantly associated with increased proteolytic activity of MMP-9 cells, contributing to increased transcriptional activation of the MMP-9 gene. Our results show that the S100A4 gene controls human CaP cells' invasive ability by regulation of MMP-9, and that this association may contribute to CaP cell metastasis. We recommend that S100A4 be used as a biomarker for CaP progression and a new therapeutic or chemopreventive target for human CaP therapy.
Source link: https://doi.org/10.1073/pnas.0606747103
Until now, the lapachol used in Tabebuia avellandae was only well known. Objective: This study was conducted to determine the inhibitory effect of lapachol on MMPs related to cell invasion. Compared to the PMA treatment group, the protein and gene expression levels of MMP-2 stimulated by PMA were significantly reduced in the presence of lapachol at 1 M. In addition, lapachol raised the expression level of TIMP-1 in comparison to the PMA control group. In addition, lapachol reduced the expression level of p-38 among MAPKs compared to the PMA treatment group. Conclusion: The above results show that lapachol may play a significant role in the modulation of MMPs related to cell invasion via TIMP-1 rise and cell activation NF-kB transcription factor, as well as the inactivation of p38 by NF-kB transcription factor.
Source link: https://doi.org/10.2174/1874467213666201005122230
Micro RNAs are small noncoding RNAs that control gene expression by binding to target messenger RNA's identical sequences. METHODS The authors investigated whether miR-22 level in human spinal DAs can be raised by using miRNA chips. The role of miR-22 in 1321N1 human astrocytoma cells was investigated next. The authors transplanted miR-22 overexpressed astrocytoma cells into mouse thoracic spinal cord, hoping to clarify whether miR-22 promotes invasion by astrocytoma cells in vivo. When transplanted into mouse spinal cord, the authors discovered that miR-22 promoted invasiveness in 1321N1 astrocytoma cells. MiR-22 appears to prevent the proliferation of 1321N1 astrocytoma cells by targeting TIMP2 expression, according to these results. To clarify the findings of this research for a novel therapeutic target for spinal DAs, this study needs additional studies with more instances and cell lines to further clarify the results.
Source link: https://doi.org/10.3171/2016.8.spine16248
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