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Open AccessJournal ArticleDOI

ARID2 Chromatin Remodeler in Hepatocellular Carcinoma

Robin Loesch, +2 more
- 23 Sep 2020 - 
- Vol. 9, Iss: 10, pp 2152
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TLDR
This review summarizes what the authors know about the tumor-modulating properties of ARID2 in hepatocellular carcinoma and discusses the molecular consequences of specific mutations impairing chromatin remodelers.
Abstract
Chromatin remodelers are found highly mutated in cancer including hepatocellular carcinoma. These mutations frequently occur in ARID (AT-rich Interactive Domain) genes, encoding subunits of the ATP-dependent SWI/SNF remodelers. The increasingly prevalent complexity that surrounds the functions and specificities of the highly modular BAF (BG1/BRM-associated factors) and PBAF (polybromo-associated BAF) complexes, including ARID1A/B or ARID2, is baffling. The involvement of the SWI/SNF complexes in diverse tissues and processes, and especially in the regulation of gene expression, multiplies the specific outcomes of specific gene alterations. A better understanding of the molecular consequences of specific mutations impairing chromatin remodelers is needed. In this review, we summarize what we know about the tumor-modulating properties of ARID2 in hepatocellular carcinoma.

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Journal ArticleDOI

3D chromatin architecture and transcription regulation in cancer

TL;DR: In this paper , a review discusses key 3D chromatin structures (topologically associating domain, lamina-associated domain, and enhancer-promoter interactions) and corresponding structural protein elements mediating 3-dimensional chromatin interactions with a highlight of their associations with cancer.
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BRD4 inhibition induces synthetic lethality in ARID2-deficient hepatocellular carcinoma by increasing DNA damage

TL;DR: It is disclosed that BRD4 inhibition may induce synthetic lethality in ARID2-deficient HCC cells, which might provide a potential therapeutic strategy for HCC patients with ARID 2 mutations.
Journal ArticleDOI

Pathogenesis and Current Treatment Strategies of Hepatocellular Carcinoma

TL;DR: In this paper , the authors presented the treatment sequences for early and advanced hepatocellular carcinoma stages according to the recently updated Barcelona Clinic Liver Cancer classification system and the current algorithm of systemic therapy (first-, second-, and third-line treatment) are summarized.
Journal ArticleDOI

ARID2 suppression promotes tumor progression and upregulates cytokeratin 8, 18 and β-4 integrin expression in TP53-mutated tobacco-related oral cancer and has prognostic implications.

TL;DR: This study is the first to demonstrate tumor suppressor role of ARID2 in TP53 mutated background indicating their cooperative role in OSCC, and also highlights its prognostic implications suggesting ARID 2 as an important therapeutic target inOSCC.
Journal ArticleDOI

Expression Signature of the AT-Rich Interactive Domain Gene Family Identified in Digestive Cancer

TL;DR: A systematic study of the ARID gene family and its association with the immune infiltrate, tumour microenvironment and outcomes of digestive cancer patients focus on the complex relations and indicate the need to study each ARID member as an individual in a specific cancer type.
References
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Hepatocellular carcinoma.

TL;DR: In this paper, the authors used non-invasive criteria to diagnose hepatocellular carcinoma (HCC) and showed that 25% of all HCCs present potentially actionable mutations, which are yet to translate into clinical practice.
Journal ArticleDOI

Cooperation between Complexes that Regulate Chromatin Structure and Transcription

TL;DR: How the activities of two major classes of chromatin-modifying complexes, ATP-dependent remodeling complexes and HAT or HDAC complexes might be coordinated to create a DNA template that is accessible to the general transcription apparatus is discussed.
Journal ArticleDOI

Truncating Mutations of hSNF5/INI1 in Aggressive Paediatric Cancer

TL;DR: The observation of bi-allelic alterations of hSNF5/INI1 in MRTs suggests that loss-of-function mutations of h snf5/inI1 contribute to oncogenesis, and the most frequently deleted part of chromosome 22q11.2 is mapped.
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