Down-modulation of Bis reduces the invasive ability of glioma cells induced by TPA, through NF-κB mediated activation of MMP-9

Lee, Young Dae; Cui, Mei Nu; Yoon, Hye Hyeon; Kim, Hye Yun; Oh, Il‐Hoan; Lee, Jeong Hwa

doi:10.5483/bmbrep.2014.47.5.172

Cited by 12 publications

(7 citation statements)

References 27 publications

(40 reference statements)

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“…The upregulation of MMP-9 expression and the downregulation of p16 expression in glioma may be associated with tumor invasiveness. MMP-9 expression was shown to be lower in non-malignant astrocytoma cells, than in anaplastic astrocytoma and glioblastoma multiforme cells exhibiting high levels of malignancy (28). High levels of MMP-9 expression may reflect the degree of malignancy and invasiveness in brain glioma.…”

Section: Discussionmentioning

confidence: 92%

Paeoniflorin inhibits proliferation and induces apoptosis of human glioma cells via microRNA-16 upregulation and matrix metalloproteinase-9 downregulation

Wei

et al. 2015

Molecular Medicine Reports

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Paeoniflorin is one of the active ingredients of the commonly used herbal medicine derived from Paeonia, which exhibits anticancer properties. MicroRNA-16 (miR-16) is upregulated in CD133(-) cells, but downregulated in CD133(+) cells from glioma tissue. Matrix metalloproteinase-9 (MMP-9) expression in glioma tissue samples is significantly higher than that in healthy brain tissue samples. Therefore, miR-16 and MMP-9 expression may be associated with glioma pathogenesis. In the present study, the effects of paeoniflorin on glioma were analyzed. U87 cells were treated with paeoniflorin at 0, 5, 10 and 20 μΜ concentrations. The results suggested that paeoniflorin inhibited U87 cell proliferation and accelerated cell apoptosis. In the present study paeoniflorin treatment increased miR-16 expression and reduced MMP-9 protein expression in U87 cells. Additionally, the results of the present study suggested that miR-16 may regulate MMP-9 expression in miR-16-transfected U87 cells. Furthermore, anti-miR-16 antibodies were used in order to investigate the apoptotic effects of paeoniflorin on U87 cells. The results demonstrated that paeoniflorin inhibits proliferation and induces apoptosis of human glial cells, via miR-16 upregulation and MMP-9 downregulation.

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Section: Discussionmentioning

confidence: 92%

Paeoniflorin inhibits proliferation and induces apoptosis of human glioma cells via microRNA-16 upregulation and matrix metalloproteinase-9 downregulation

Wei

et al. 2015

Molecular Medicine Reports

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“…However, levels of E-cadherin, an epithelial marker, were notably higher in BIS-depleted cells, indicating that BIS depletion retarded the EMT process though regulation of the expression of several genes. Since BIS enhances the activities of MMP-2 [26, 27] and MMP-9 [40], which are representative STAT3 targets [41], we measured the mRNA levels of these genes. As shown in Figure 6B, MMP-2 mRNA levels significantly decreased in si-BIS-treated A172 spheres, but MMP-9 levels remained unchanged (data not shown).…”

Section: Resultsmentioning

confidence: 99%

BIS-mediated STAT3 stabilization regulates glioblastoma stem cell-like phenotypes

Yun

Song

et al. 2016

Oncotarget

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Glioblastoma stem cells (GSCs) are a subpopulation of highly tumorigenic and stem-like cells that are responsible for resistance to conventional therapy. Bcl-2-intreacting cell death suppressor (BIS; also known as BAG3) is an anti-apoptotic protein that is highly expressed in human cancers with various origins, including glioblastoma. In the present study, to investigate the role of BIS in GSC subpopulation, we examined the expression profile of BIS in A172 and U87-MG glioblastoma cell lines under specific in vitro culture conditions that enrich GSC-like cells in spheres. Both BIS mRNA and protein levels significantly increased under the sphere-forming condition as compared with standard culture conditions. BIS depletion resulted in notable decreases in sphere-forming activity and was accompanied with decreases in SOX-2 expression. The expression of STAT3, a master regulator of stemness, also decreased following BIS depletion concomitant with decreases in the nuclear levels of active phosphorylated STAT3, while ectopic STAT3 overexpression resulted in recovery of sphere-forming activity in BIS-knockdown glioblastoma cells. Additionally, immunoprecipitation and confocal microscopy revealed that BIS physically interacts with STAT3. Furthermore, BIS depletion increased STAT3 ubiquitination, suggesting that BIS is necessary for STAT3 stabilization in GSC-like cells. BIS depletion also affected epithelial-to-mesenchymal transition-related genes as evidenced by decrease in SNAIL and MMP-2 expression and increase in E-cadherin expression in GSC-like cells. Our findings suggest that high levels of BIS expression might confer stem-cell-like properties on cancer cells through STAT3 stabilization, indicating that BIS is a potential target in cancer therapy.

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“…This study examined the combined effects of serum deprivation and culture plate surface type on the morphology, viability, and markers for stemness and EMT in A172 glioblastoma cells. These cells were previously shown to have aggressive migration ability and ROS accumulation in response to appropriate stimuli (36,37).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of SOX-2 expression and ROS accumulation by culture of A172 glioblastoma cells under non-adherent culture conditions

Yun

Yoo

et al. 2015

Oncology Reports

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More efficient isolation and identification of cancer stem cells (CSCs) would help in determining their fundamental roles in tumor biology. The classical tool for this purpose is anchorage-independent tumorsphere culture. We compared the effects of differently textured culture plates and serum deprivation on the acquisition of CSC properties of A172 glioblastoma cells. Cells were cultured on standard polystyrene-treated plates, ultra-low attachment, poly (2-hydroxyethyl methacrylate)-coated plates, and 1% agar-coated plates with 10% serum or in serum-free glioblastoma sphere medium (GBM). Based on mitochondrial reductase activity and subG1 proportions, non-adherent conditions had a greater impact on A172 cell viability than serum deprivation. Among the stemness-related genes, SOX-2 expression was significantly upregulated by serum deprivation under non-adherent conditions, while several epithelial-to-mesenchymal transition (EMT)-related genes were less dependent on serum. In addition, reactive oxygen species (ROS) accumulation in A172 cells was significantly increased in GBM under non-adherent conditions. Despite the correlation between SOX-2 induction and ROS accumulation, treatment with the ROS scavenger N-acetyl-l-cysteine did not prevent SOX-2 expression, suggesting that ROS accumulation is not an essential requirement for induction of SOX-2. Our results suggested that cultivation of cancer cells under conditions of serum deprivation in an anchorage-independent manner may enrich SOX-2-expressing CSC-like cells in vitro.

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Down-modulation of Bis reduces the invasive ability of glioma cells induced by TPA, through NF-κB mediated activation of MMP-9

Cited by 12 publications

References 27 publications

Paeoniflorin inhibits proliferation and induces apoptosis of human glioma cells via microRNA-16 upregulation and matrix metalloproteinase-9 downregulation

Paeoniflorin inhibits proliferation and induces apoptosis of human glioma cells via microRNA-16 upregulation and matrix metalloproteinase-9 downregulation

BIS-mediated STAT3 stabilization regulates glioblastoma stem cell-like phenotypes

Enhancement of SOX-2 expression and ROS accumulation by culture of A172 glioblastoma cells under non-adherent culture conditions

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