Targeting the anaphase-promoting complex/cyclosome (APC/C)- bromodomain containing 7 (BRD7) pathway for human osteosarcoma

Hu, Kaishun; Liao, Dan; Wu, Wenjing; Han, An Jia; Shi, Hui; Wang, Fen; Wang, Xin; Zhong, Li; Duan, Tingmei; Wu, Yuanzhong; Jie, Cao; Tang, Jianjun; Sang, Yi; Wang, Li; Lv, Xiaobin; Xu, Shuangbing; Zhang, Ru Hua; Deng, Wu; Li, Sheng Ping; Zeng, Yi Xin; Kang, Tiebang

doi:10.18632/oncotarget.1816

Cited by 30 publications

(37 citation statements)

References 36 publications

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“…Accumulating evidence demonstrates that inactivation of the BRD7 gene contributes to the development of many human cancers by transcriptional dysregulation [1,2,[6][7][8][9][10][11][12][13]. BRD7 regulates signaling pathways that involve cell growth, apoptosis, cell cycle, and mobility [14][15][16][17][18][19][20][21].…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicates that BRD7 was also down-regulated in multiple types of human cancer, including breast [6], prostate [7], endometrial [8], colorectal [9], ovarian [10], and pancreas cancer [11], glioma [12], and osteosarcoma [13]. BRD7 can inhibit cell growth through multiple mechanisms, including cell cycle arrest and apoptosis [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Xiong

Zhou

et al. 2015

Mol Cell Biochem

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BRD7 is a single bromodomain-containing protein that functions as a subunit of the SWI/SNF chromatin-remodeling complex to regulate transcription. It also interacts with the well-known tumor suppressor protein p53 to trans-activate genes involved in cell cycle arrest. In this paper, we report an integrative analysis of genome-wide chromatin occupancy of BRD7 by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and digital gene expression (DGE) profiling by RNA-sequencing upon the overexpression of BRD7 in human cells. We localized 156 BRD7-binding peaks representing 184 genes by ChIP-sequencing, and most of these peaks were co-localized with histone modification sites. Four novel motifs were significantly represented in these BRD7-enriched regions. Ingenuity pathway analysis revealed that 22 of these BRD7 target genes were involved in a network regulating cell death and survival. DGE profiling identified 560 up-regulated genes and 1088 down-regulated genes regulated by BRD7. Using Gene Ontology and pathway analysis, we found significant enrichment of the cell cycle and apoptosis pathway genes. For the integrative analysis of the ChIP-seq and DEG data, we constructed a regulating network of BRD7 downstream genes, and this network suggests multiple feedback regulations of the pathways. Furthermore, we validated BIRC2, BIRC3, TXN2, and NOTCH1 genes as direct, functional BRD7 targets, which were involved in the cell cycle and apoptosis pathways. These results provide a genome-wide view of chromatin occupancy and the gene regulation network of the BRD7 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Xiong

Zhou

et al. 2015

Mol Cell Biochem

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“…It has been found to inhibit the cell cycle G1-S phase progression, initiate apoptosis and reverse cellular malignancy through the ras/MEK/ERK, Rb/E2F and Wnt signaling pathways. [1][2][3][4] BRD7 is a member of the bromodomain family, which includes BRD2, BRD3, BRD9 and BRDT, [5][6][7] and can recognize and bind to acetylated histone H3. 8 BRD7 is primarily localized in the nucleus and possesses a functional nuclear localization signal sequence.…”

Section: Introductionmentioning

confidence: 99%

BRD7 plays an anti-inflammatory role during early acute inflammation by inhibiting activation of the NF-кB signaling pathway

et al. 2016

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Increasing evidence has shown a strong association between tumor-suppressor genes and inflammation. However, the role of BRD7 as a novel tumor suppressor in inflammation remains unknown. In this study, by observing BRD7 knockout mice for 6-12 months, we discovered that compared with BRD7 mice, BRD7 mice were more prone to inflammation, such as external inflammation and abdominal abscess. By using mouse embryo fibroblast (MEF) cells from the BRD7 knockout mouse, an in vitro lipopolysaccharide (LPS)-stimulated MEF cell line was established. The mRNA levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), chemokine (C-X-C motif) ligand 1 (CXCL-1) and inducible nitric oxide synthase (iNOS) were significantly increased in BRD7 MEF cells compared with BRD7 MEF cells after LPS stimulation for 1 or 6 h. In addition, the cytoplasm-to-nucleus translocation of nuclear factor kappa-B (NF-κB; p65) and an increased NF-κB reporter activity were observed in BRD7 MEF cells at the 1 h time point but not at the 6 h time point. Furthermore, an in vivo dextran sodium sulfate (DSS)-induced acute colitis model was created. As expected, the disease activity index (DAI) value was significantly increased in the BRD7 mice after DSS treatment for 1-5 days, which was demonstrated by the presence of a significantly shorter colon, splenomegaly and tissue damage. Moreover, higher expression levels of IL-6, TNF-α, p65, CXCL-1 and iNOS, and an increased level of NF-κB (p65) nuclear translocation were also found in the DSS-treated BRD7 mice. These findings suggest that BRD7 has an anti-inflammatory role during early acute inflammation by inhibiting activation of the NF-кB signaling pathway, which provides evidence to aid in understanding the therapeutic effects of BRD7 on inflammatory diseases.

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“…Using the bioinformatics tool (Targetscan), we demonstrated that miR‐410 bound to the 3′‐UTR of BRD7. BRD7 is downregulated in various malignancies, which encourage us to believe that BRD7 may be a miR‐410 direct target in NSCLC [39–41]. In addition, miR‐410 inhibited BRD7 mRNA and protein expression.…”

Section: Discussionmentioning

confidence: 97%

MicroRNA‐410 promotes cell proliferation by targeting BRD7 in non‐small cell lung cancer

Yang

Zhu

et al. 2015

FEBS Letters

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Edited by Tamas DalmayKeywords: Non-small cell lung cancer microRNA miR-410 Bromodomain-containing protein 7 a b s t r a c t miR-410 acts as an oncogene or tumor suppressor gene in some malignancies. However, its role in NSCLC is still unknown. In this study, we showed that the expression of miR-410 was up-regulated in both human NSCLC tissues and cells. Overexpression of miR-410 promoted cell proliferation, migration, and invasion of NSCLC. In addition, bromodomain-containing protein 7 (BRD7) was a direct target of miR-410. MiR-410-mediated downregulation of BRD7 led to increase Akt phosphorylation. Inhibition of Akt phosphorylation can rescue the effect of miR-410 on NSCLC cell. The expression of BRD7 was downregulated in NSCLC and was inversely expressed with miR-410 in NSCLC. Our data provided new knowledge regarding the role of miR-410 in the lung cancer progression.

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Targeting the anaphase-promoting complex/cyclosome (APC/C)- bromodomain containing 7 (BRD7) pathway for human osteosarcoma

Cited by 30 publications

References 36 publications

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

BRD7 plays an anti-inflammatory role during early acute inflammation by inhibiting activation of the NF-кB signaling pathway

MicroRNA‐410 promotes cell proliferation by targeting BRD7 in non‐small cell lung cancer

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