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      BRD7 Acts as a Tumor Suppressor Gene in Lung Adenocarcinoma

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      Author(s): , , *
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      Journal: PLoS ONE
      Publisher: Public Library of Science

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          Abstract

          Lung cancer is one of the most malignant tumors and the leading cause of cancer-related deaths worldwide. Among lung cancers, 40% are diagnosed as adenocarcinoma. Bromodomain containing 7 (BRD7) is a member of bromodomain-containing protein family. It was proved to be downregulated in various cancers. However, the role of BRD7 in lung adenocarcinoma is still unknown. Western blot and qRT-PCR was performed to measure the BRD7 expression in lung adenocarcinoma tissues and cells. CCK8 and migration assay was done to detect the functional role of BRD7 in lung adenocarcinoma. In this study, we showed that the expression of BRD7 was downregulated in lung adenocarcinoma tissues and cells. The lower of BRD7 levels in patients with lung adenocarcinoma was associated with shortened disease-free survival. Furthermore, overexpression of BRD7 inhibited lung adenocarcinoma cell proliferation and migration. Inhibition of BRD7 expression promoted cell proliferation and migration by activating ERK phosphorylation. Overexpression of BRD7 inhibited cyclin D and myc expression. Our findings are consistent with a tumor suppressor role for BRD7 in lung adenocarcinoma tumorigenesis.

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          Molecular portraits of epithelial, mesenchymal, and hybrid States in lung adenocarcinoma and their relevance to survival.

          Mark Schliekelman, Ayumu Taguchi, Jun Zhu … (2015)
          Epithelial-to-mesenchymal transition (EMT) is a key process associated with tumor progression and metastasis. To define molecular features associated with EMT states, we undertook an integrative approach combining mRNA, miRNA, DNA methylation, and proteomic profiles of 38 cell populations representative of the genomic heterogeneity in lung adenocarcinoma. The resulting data were integrated with functional profiles consisting of cell invasiveness, adhesion, and motility. A subset of cell lines that were readily defined as epithelial or mesenchymal based on their morphology and E-cadherin and vimentin expression elicited distinctive molecular signatures. Other cell populations displayed intermediate/hybrid states of EMT, with mixed epithelial and mesenchymal characteristics. A dominant proteomic feature of aggressive hybrid cell lines was upregulation of cytoskeletal and actin-binding proteins, a signature shared with mesenchymal cell lines. Cytoskeletal reorganization preceded loss of E-cadherin in epithelial cells in which EMT was induced by TGFβ. A set of transcripts corresponding to the mesenchymal protein signature enriched in cytoskeletal proteins was found to be predictive of survival in independent datasets of lung adenocarcinomas. Our findings point to an association between cytoskeletal and actin-binding proteins, a mesenchymal or hybrid EMT phenotype and invasive properties of lung adenocarcinomas.
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            BRD7, a novel PBAF-specific SWI/SNF subunit, is required for target gene activation and repression in embryonic stem cells.

            John Yates III, Donna M Kaeser, Aaron Aslanian … (2008)
            The composition of chromatin-remodeling complexes dictates how these enzymes control transcriptional programs and cellular identity. In the present study we investigated the composition of SWI/SNF complexes in embryonic stem cells (ESCs). In contrast to differentiated cells, ESCs have a biased incorporation of certain paralogous SWI/SNF subunits with low levels of BRM, BAF170, and ARID1B. Upon differentiation, the expression of these subunits increases, resulting in a higher diversity of compositionally distinct SWI/SNF enzymes. We also identified BRD7 as a novel component of the Polybromo-associated BRG1-associated factor (PBAF) complex in both ESCs and differentiated cells. Using short hairpin RNA-mediated depletion of BRG1, we showed that SWI/SNF can function as both a repressor and an activator in pluripotent cells, regulating expression of developmental modifiers and signaling components such as Nodal, ADAMTS1, BMI-1, CRABP1, and thyroid releasing hormone. Knockdown studies of PBAF-specific BRD7 and of a signature subunit within the BAF complex, ARID1A, showed that these two subcomplexes affect SWI/SNF target genes differentially, in some cases even antagonistically. This may be due to their different biochemical properties. Finally we examined the role of SWI/SNF in regulating its target genes during differentiation. We found that SWI/SNF affects recruitment of components of the preinitiation complex in a promoter-specific manner to modulate transcription positively or negatively. Taken together, our results provide insight into the function of compositionally diverse SWI/SNF enzymes that underlie their inherent gene-specific mode of action.
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              BRD7 is a candidate tumour suppressor gene required for p53 function.

              Francesca Tocco, F Mantovani, Giannino Del Sal … (2010)
              Oncogene-induced senescence is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations and others show a dysfunctional p53 pathway, frequently by unknown mechanisms. Here we identify BRD7 (bromodomain-containing 7) as a protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. In human breast tumours harbouring wild-type, but not mutant, p53 the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300 and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation and promoter activity. Thus, BRD7 suppresses tumorigenicity by serving as a p53 cofactor required for the efficient induction of p53-dependent oncogene-induced senescence.
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                Author and article information

                Contributors
                Srikumar Chellappan: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 31 August 2016
                Publication date Collection: 2016
                Volume: 11
                Issue: 8
                Electronic Location Identifier: e0156701
                Affiliations
                [001]Department of thoracic surgical oncology, cancer institute (hospital), Chinese academy of medical sciences, Peking union medical college, Beijing, 100021, China
                H. Lee Moffitt Cancer Center & Research Institute, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                • Conceived and designed the experiments: YG BW SG.

                • Performed the experiments: YG BW SG.

                • Analyzed the data: YG BW SG.

                • Contributed reagents/materials/analysis tools: YG BW SG.

                • Wrote the paper: YG BW SG.

                Article
                Publisher ID: PONE-D-16-07186
                DOI: 10.1371/journal.pone.0156701
                PMC ID: 5007050
                PubMed ID: 27580131
                SO-VID: b1070bb7-e2ef-4f58-adf0-d82ab5bddb3e
                Copyright © © 2016 Gao et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 19 February 2016
                Date accepted : 18 May 2016
                Page count
                Figures: 6, Tables: 0, Pages: 9
                Funding
                The authors received no specific funding for this work.
                Categories
                Subject: Research Article
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Carcinomas
                Subject: Adenocarcinomas
                Subject: Adenocarcinoma of the Lung
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Lung and Intrathoracic Tumors
                Subject: Adenocarcinoma of the Lung
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Carcinomas
                Subject: Adenocarcinomas
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Lung and Intrathoracic Tumors
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Lung and Intrathoracic Tumors
                Subject: Secondary Lung Tumors
                Subject: Biology and Life Sciences
                Subject: Genetics
                Subject: Gene Expression
                Subject: Biology and Life Sciences
                Subject: Molecular Biology
                Subject: Molecular Biology Techniques
                Subject: Molecular Biology Assays and Analysis Techniques
                Subject: Gene Expression and Vector Techniques
                Subject: Hyperexpression Techniques
                Subject: Research and Analysis Methods
                Subject: Molecular Biology Techniques
                Subject: Molecular Biology Assays and Analysis Techniques
                Subject: Gene Expression and Vector Techniques
                Subject: Hyperexpression Techniques
                Subject: Research and Analysis Methods
                Subject: Biological Cultures
                Subject: Cell Cultures
                Subject: Cultured Tumor Cells
                Subject: Adenocarcinoma Cells
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cell Motility
                Subject: Cell Migration
                Subject: Biology and Life Sciences
                Subject: Developmental Biology
                Subject: Cell Migration
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                Data Availability All relevant data are within the paper.

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