BRMS1 Suppresses Glioma Progression by Regulating Invasion, Migration and Adhesion of Glioma Cells

Mei, Peng-jin; Bai, Jing; Shi, Meilin; Liu, Qinghua; Li, Zhonglin; Fan, Yi‐Ming; Zheng, Junnian

doi:10.1371/journal.pone.0098544

Cited by 21 publications

(25 citation statements)

References 38 publications

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“…In addition, the overexpression of p40 significantly inhibits human cell growth [29]. In this study, the expression value of BRMS1L was down-regulated, which is consistent with the previous studies about BRMS1 and p40 [27,29]. These findings indicated that BRMS1L might play a GAPN glioma associated protein-protein interaction network Fig.…”

Section: Discussionsupporting

confidence: 91%

“…However, BRMS1L codes a family of breast cancer metastasis suppressor 1-like (BRMS1L) proteins. Breast cancer metastasis suppressor 1 (BRMS1) is a member of the mSin3-HDAC transcription corepressor complex [26], and is significantly down-regulated in glioma compared with adjacent non-tumor tissue [27]. The overexpression of BRMS1 inhibits glioma cell invasion, migration, and adhesion capacity by suppressing NF-κB, uPA, MMP-2, and Src-FAK pathway [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Breast cancer metastasis suppressor 1 (BRMS1) is a member of the mSin3-HDAC transcription corepressor complex [26], and is significantly down-regulated in glioma compared with adjacent non-tumor tissue [27]. The overexpression of BRMS1 inhibits glioma cell invasion, migration, and adhesion capacity by suppressing NF-κB, uPA, MMP-2, and Src-FAK pathway [27,28]. Furthermore, among the BRMS1L proteins, p40 is also a component of the mSin3A/p33(ING1b)/HDAC1 deacetylase complex, which binds to the promoters of target genes, and represses gene transcription [29].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Revealing the Potential Pathogenesis of Glioma by Utilizing a Glioma Associated Protein-Protein Interaction Network

Pan

Yang

et al. 2014

Pathol. Oncol. Res.

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This study aims to explore the potential mechanism of glioma through bioinformatic approaches. The gene expression profile (GSE4290) of glioma tumor and non-tumor samples was downloaded from Gene Expression Omnibus database. A total of 180 samples were available, including 23 non-tumor and 157 tumor samples. Then the raw data were preprocessed using robust multiarray analysis, and 8,890 differentially expressed genes (DEGs) were identified by using t-test (false discovery rate < 0.0005). Furthermore, 16 known glioma related genes were abstracted from Genetic Association Database. After mapping 8,890 DEGs and 16 known glioma related genes to Human Protein Reference Database, a glioma associated protein-protein interaction network (GAPN) was constructed. In addition, 51 sub-networks in GAPN were screened out through Molecular Complex Detection (score ≥ 1), and sub-network 1 was found to have the closest interaction (score = 3). What' more, for the top 10 sub-networks, Gene Ontology (GO) enrichment analysis (p value < 0.05) was performed, and DEGs involved in sub-network 1 and 2, such as BRMS1L and CCNA1, were predicted to regulate cell growth, cell cycle, and DNA replication via interacting with known glioma related genes. Finally, the overlaps of DEGs and human essential, housekeeping, tissue-specific genes were calculated (p value = 1.0, 1.0, and 0.00014, respectively) and visualized by Venn Diagram package in R. About 61% of human tissue-specific genes were DEGs as well. This research shed new light on the pathogenesis of glioma based on DEGs and GAPN, and our findings might provide potential targets for clinical glioma treatment.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Revealing the Potential Pathogenesis of Glioma by Utilizing a Glioma Associated Protein-Protein Interaction Network

Pan

Yang

et al. 2014

Pathol. Oncol. Res.

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show abstract

“…BRMS1 also regulates a network of proteins with central roles in cancer metastasis (19,34). For instance, Mei et al (35) demonstrated that BRMS1 was able to inhibit the invasion of glioma cells by suppressing urokinase-type plasminogen activator, nuclear factor-κB and the expression and enzymatic activity of matrix metalloproteinase-2 (MMP-2). You et al (36) reported that BRMS1 is able to regulate apoptosis in NSCLC cells by modulating the activation of signal transducer and activator of transcription 3.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑125a‑5p inhibits invasion and metastasis of gastric cancer cells by targeting BRMS1 expression

Cao

Tan

et al. 2018

Oncol Lett

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Abstract. Accumulating studies have demonstrated microRNAs (miRNAs/miRs) have an important role in multiple processes of human malignant tumor development and progression. Decreased expression of miR-125a-5p has been observed in several types of cancer, including gastric cancer (GC). However, the mechanism and exact function of miR-125a-5p in GC have not been largely elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction indicated that the expression of miR-125a-5p was downregulated in GC tissues and cell lines compared with matched normal tissues (P<0.01) and normal gastric mucosa cell lines (P<0.01), respectively. Moreover, clinical pathological characteristics and Kaplan-Meier analysis indicated that a low expression of miR-125a-5p was not only associated with lymph metastasis, peritoneal dissemination and advanced tumor-node metastasis stage but also affected the prognosis of GC patients. Compared with miR-control-transfected GC cells, markedly decreased migration and invasion was observed in GC cells that overexpress miR-125a-5p. By contrast, increased metastasis and invasion were observed in miR-125a-5p-knocked down cells compared with the control. Furthermore, luciferase reporter assays indicated that breast cancer metastasis suppressor 1 (BRMS1) was a direct target of miR-125a-5p. Notably, a positive correlation between the levels of BRMS1 and miR-125a-5p in GC tissues was observed, and BRMS1 expression was indicated to be regulated by miR-125a-5p in GC cells. In conclusion, miR-125a-5p may act as a tumor suppressor by targeting the metastasis-inhibitory gene, BRMS1. The data suggesting that BRMS1 is a potential target gene of miR-125a-5p, may provide novel insight into miRNA regulation of human gene expression, and a useful target for gene therapy of GC.

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“…64 Motility was quantified as the percentage of the initial wound distance covered by the cells after 24 h. Consistent with previous studies, expression of wild-type BRMS1 significantly reduced the ability of MDA-MB-231 cells to migrate. [65][66][67] Therefore, while vector control MDA-MB-231 cells covered 81.3 % of the wound area within 24 hours, MDA-MB-231 cells expressing wild-type BRMS1 only covered 57.7% of the wound area ( Fig. 3A).…”

Section: Phosphorylation Of Brms1 On Serine 237 Affects Cell Migrationmentioning

confidence: 97%

Cyclin-dependent kinase-mediated phosphorylation of breast cancer metastasis suppressor 1 (BRMS1) affects cell migration

et al. 2016

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Expression of Breast Cancer Metastasis Suppressor 1 (BRMS1) reduces the incidence of metastasis in many human cancers, without affecting tumorigenesis. BRMS1 carries out this function through several mechanisms, including regulation of gene expression by binding to the mSin3/histone deacetylase (HDAC) transcriptional repressor complex. In the present study, we show that BRMS1 is a novel substrate of Cyclin-Dependent Kinase 2 (CDK2) that is phosphorylated on serine 237 (S237). Although CDKs are known to regulate cell cycle progression, the mutation of BRMS1 on serine 237 did not affect cell cycle progression and proliferation of MDA-MB-231 breast cancer cells; however, their migration was affected. Phosphorylation of BRMS1 does not affect its association with the mSin3/HDAC transcriptional repressor complex or its transcriptional repressor activity. The serine 237 phosphorylation site is immediately proximal to a C-terminal nuclear localization sequence that plays an important role in BRMS1-mediated metastasis suppression but phosphorylation does not control BRMS1 subcellular localization. Our studies demonstrate that CDK-mediated phosphorylation of BRMS1 regulates the migration of tumor cells.

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BRMS1 Suppresses Glioma Progression by Regulating Invasion, Migration and Adhesion of Glioma Cells

Cited by 21 publications

References 38 publications

Revealing the Potential Pathogenesis of Glioma by Utilizing a Glioma Associated Protein-Protein Interaction Network

Revealing the Potential Pathogenesis of Glioma by Utilizing a Glioma Associated Protein-Protein Interaction Network

MicroRNA‑125a‑5p inhibits invasion and metastasis of gastric cancer cells by targeting BRMS1 expression

Cyclin-dependent kinase-mediated phosphorylation of breast cancer metastasis suppressor 1 (BRMS1) affects cell migration

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