Oncogene-dependent function of BRG1 in hepatocarcinogenesis

Wang, Pan; Song, Xinhua; Cao, Dan; Cui, Kairong; Wang, Jingxiao; Utpatel, Kirsten; Shang, Runze; Wang, Haichuan; Che, Li; Evert, Matthias; Zhao, Keji; Calvisi, Diego F.; Chen, Xin

doi:10.1038/s41419-020-2289-3

Cited by 31 publications

(31 citation statements)

References 45 publications

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“…Bai and colleagues showed that knockdown of BRG1 by RNAi greatly reduced breast cancer cell proliferation and induced cell cycle arrest [ 144 ]. BRG1 overexpression in human hepatocellular carcinoma samples further suggests that BRG1 can function in both tumor suppressing and oncogenic capacities depending upon oncogenic stimuli [ 145 ]. The potential therapeutic effects of targeting of BRG1 ATPase activity were recently assessed [ 146 , 147 ].…”

Section: Gbaf and Its Subunits In Mammalian Diseasementioning

confidence: 99%

GBAF, a small BAF sub-complex with big implications: a systematic review

Innis

Cabot

2020

Epigenetics & Chromatin

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ATP-dependent chromatin remodeling by histone-modifying enzymes and chromatin remodeling complexes is crucial for maintaining chromatin organization and facilitating gene transcription. In the SWI/SNF family of ATP-dependent chromatin remodelers, distinct complexes such as BAF, PBAF, GBAF, esBAF and npBAF/nBAF are of particular interest regarding their implications in cellular differentiation and development, as well as in various diseases. The recently identified BAF subcomplex GBAF is no exception to this, and information is emerging linking this complex and its components to crucial events in mammalian development. Furthermore, given the essential nature of many of its subunits in maintaining effective chromatin remodeling function, it comes as no surprise that aberrant expression of GBAF complex components is associated with disease development, including neurodevelopmental disorders and numerous malignancies. It becomes clear that building upon our knowledge of GBAF and BAF complex function will be essential for advancements in both mammalian reproductive applications and the development of more effective therapeutic interventions and strategies. Here, we review the roles of the SWI/SNF chromatin remodeling subcomplex GBAF and its subunits in mammalian development and disease.

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Section: Gbaf and Its Subunits In Mammalian Diseasementioning

confidence: 99%

GBAF, a small BAF sub-complex with big implications: a systematic review

Innis

Cabot

2020

Epigenetics & Chromatin

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“…It is of intrigue to note that there appears to be a striking similarity in terms of the pathobiological processes that BRG1 and CK2 seem to co-regulate although no prior study has ever linked one to the other. BRG1 and CK2 can both regulate SREBP-dependent lipogenesis [ 35 , 98 ], liver regeneration [ 32 , 99 ], and hepatocellular carcinoma [ 100 , 101 ]. Further studies are warranted to address whether there is a universal co-dependency between BRG1 and CK2 in liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Redox-sensitive activation of CCL7 by BRG1 in hepatocytes during liver injury

et al. 2021

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Liver injuries induced by various stimuli share in common an acute inflammatory response, in which circulating macrophages home to the liver parenchyma to participate in the regulation of repair, regeneration, and fibrosis. In the present study we investigated the role of hepatocyte-derived C–C motif ligand 7 (CCL7) in macrophage migration during liver injury focusing on its transcriptional regulation. We report that CCL7 expression was up-regulated in the liver by lipopolysaccharide (LPS) injection (acute liver injury) or methionine-and-choline-deficient (MCD) diet feeding (chronic liver injury) paralleling increased macrophage infiltration. CCL7 expression was also inducible in hepatocytes, but not in hepatic stellate cells or in Kupffer cells, by LPS treatment or exposure to palmitate in vitro . Hepatocyte-specific deletion of Brahma-related gene 1 (BRG1), a chromatin remodeling protein, resulted in a concomitant loss of CCL7 induction and macrophage infiltration in the murine livers. Of interest, BRG1-induced CCL7 transcription and macrophage migration was completely blocked by the antioxidant N-acetylcystine. Further analyses revealed that BRG1 interacted with activator protein 1 (AP-1) to regulate CCL7 transcription in hepatocytes in a redox-sensitive manner mediated in part by casein kinase 2 (CK2)-catalyzed phosphorylation of BRG1. Importantly, a positive correlation between BRG1/CCL7 expression and macrophage infiltration was identified in human liver biopsy specimens. In conclusion, our data unveil a novel role for BRG1 as a redox-sensitive activator of CCL7 transcription.

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“…Chromatin remodeling is essential for gene transcription, DNA replication, and DNA repair [ 78 ] that is governed by multiple protein complexes. Mutations in chromatin regulator SMARCA4, AT-rich interaction domain (ARID) 1A, ARID1B, ARID2, myeloid/lymphoid leukemia (MLL), MLL3, and bromodomain PHD finger transcription factor (BPTF) genes contribute to HCC [ 79 , 80 ].…”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

Mechanisms by Which Probiotic Bacteria Attenuate the Risk of Hepatocellular Carcinoma

Thilakarathna

Rupasinghe

Ridgway

2021

IJMS

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Hepatocellular carcinoma (HCC) is the most common primary liver cancer and the second leading cause of cancer-related deaths worldwide. Chronic infections with hepatitis B virus (HBV) and hepatitis C virus (HCV), alcoholic liver disease (ALD), and non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) are the major extrinsic risk factors of HCC development. Genetic background is pivotal in HCC pathogenesis, and both germline mutations and single nucleotide polymorphism (SNP) are intrinsic risk factors of HCC. These HCC risk factors predispose to hepatic injury and subsequent activation of fibrogenesis that progresses into cirrhosis and HCC. Probiotic bacteria can mitigate HCC risk by modulating host gut microbiota (GM) to promote growth of beneficial microbes and inhibit HCC-associated dysbiosis, thus preventing pathogen-associated molecular patterns (PAMPs)-mediated hepatic inflammation. Probiotics have antiviral activities against HBV and HCV infections, ameliorate obesity and risk of NAFLD/NASH, and their antioxidant, anti-proliferative, anti-angiogenic, and anti-metastatic effects can prevent the HCC pathogenesis. Probiotics also upregulate the expression of tumor suppressor genes and downregulate oncogene expression. Moreover, metabolites generated by probiotics through degradation of dietary phytochemicals may mitigate the risk of HCC development. These multiple anticancer mechanisms illustrate the potential of probiotics as an adjuvant strategy for HCC risk management and treatment.

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Oncogene-dependent function of BRG1 in hepatocarcinogenesis

Cited by 31 publications

References 45 publications

GBAF, a small BAF sub-complex with big implications: a systematic review

GBAF, a small BAF sub-complex with big implications: a systematic review

Redox-sensitive activation of CCL7 by BRG1 in hepatocytes during liver injury

Mechanisms by Which Probiotic Bacteria Attenuate the Risk of Hepatocellular Carcinoma

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