ARID2 Chromatin Remodeler in Hepatocellular Carcinoma

Loesch, Robin; Chenane, Linda; Colnot, Sabine

doi:10.3390/cells9102152

Cited by 16 publications

(9 citation statements)

References 79 publications

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“…Bioinformatics analysis of public databases and expression analysis of LIHC tissue samples showed that ARID4B was highly expressed in LIHC compared with adjacent normal tissues and strongly correlated with clinical features ( 35 ). The expression of ARID1A and ARID2 inhibited the proliferation and migration of LIHC cells and, thus, act as tumour suppressors ( 36 , 37 ). Therefore, the predicted roles of the ARID gene family members as a tumour suppressor or promoter in LIHC were in accord with our results, but validation from further experiments is required for an in-depth exploration.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Wang

et al. 2022

Front. Med.

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BackgroundThe AT-rich interactive domain (ARID) gene family of 15 proteins has an important role in development and proliferation. Gene expression alterations of the ARID family are correlated with the pathogenesis of digestive cancer, but systematic research has not been conducted.MethodsWe obtained transcriptome sequencing data, clinical characteristics and stemness indices of the seven main types of digestive cancer (cholangiocarcinoma, colon adenocarcinoma, oesophageal carcinoma, liver hepatocellular carcinoma, pancreatic adenocarcinoma, rectum adenocarcinoma and stomach adenocarcinoma) from public pan-cancer data to combine the analysis of the expression and prognostic signature of the ARID gene family. The stromal and immune scores for each sample were calculated to explore the correlations between the ARID gene family members and the tumour microenvironment.ResultsAfter screening, 1,920 digestive cancer samples were included in our study. ARID3C was expressed at low levels throughout the digestive cancer samples. The expression levels of ARID1A and JARID1C were relatively high, but there was striking heterogeneity across the different cancer types for specific family members. The survival analysis indicated that many genes were significantly related to the prognosis of patients with liver hepatocellular carcinoma. The stemness indices, stromal score, and immune score analysis showed that the expression of a single ARID gene had characteristic consistency in each tumour, but the levels among the different genes still varied.ConclusionOur 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.

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Section: Discussionmentioning

confidence: 99%

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

Liu

Wang

et al. 2022

Front. Med.

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“…Mutations of the ARID2 gene, which is involved in chromatin remodeling gene, are found in many human cancers. 51 , 52 In HCC, ARID2 mutations are reported to occur more frequently in HCV‐induced HCCs (6/43) in comparison to HBV‐related (1/50) and non‐viral‐related (2/44) HCC. 53 In our results, ARID2 mutations were observed in HCV‐positive tumors (6/34) and in HCV‐SVR tumors (1/35).…”

Section: Discussionmentioning

confidence: 99%

“…Mutations in ARID2 were significantly less frequent in HCV‐SVR tumors than in HCV‐positive tumors. Mutations of the ARID2 gene, which is involved in chromatin remodeling gene, are found in many human cancers 51,52 . In HCC, ARID2 mutations are reported to occur more frequently in HCV‐induced HCCs (6/43) in comparison to HBV‐related (1/50) and non‐viral‐related (2/44) HCC 53 .…”

Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma after a sustained virological response by direct‐acting antivirals harborsTP53inactivation

et al. 2022

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Introduction The genomic characteristics of hepatocellular carcinoma (HCC) after a sustained virological response (SVR) and its differences according to whether an SVR was achieved by treatment with direct‐acting antivirals (DAA) or interferon (IFN) are still not fully understood. Methods Sixty‐nine surgically resected HCCs from patients with hepatitis C virus infection were analyzed by gene expression profiling and whole‐exome sequencing. Results Among the 69 HCC patients, 34 HCCs in which an SVR was not achieved at the time of surgery were classified as HCV‐positive, and 35 HCCs in which an SVR was achieved at the time of surgery were classified as HCV‐SVR. According to the HCV treatment, 35 HCV‐SVR HCCs were classified into two groups: eight tumors with DAA (HCV‐SVR‐DAA) and 24 tumors with interferon (HCV‐SVR‐IFN). The frequency of samples with ARID2 mutations was significantly lower in HCV‐SVR than in HCV‐positive tumors ( p = 0.048). In contrast, the frequency of samples with PREX2 mutations was significantly higher in HCV‐SVR samples than in HCV‐positive samples ( p = 0.048). Among the patients with HCV‐SVR, the frequency of samples with TP53 mutations was significantly higher in HCV‐SVR‐DAA tumors than in HCV‐SVR‐IFN tumors ( p = 0.030). TP53 inactivation scores in HCV‐SVR‐DAA tumors were found to be significantly enhanced in comparison to HCV‐SVR‐IFN tumors ( p = 0.022). In addition, chromosomal instability and PI3K/AKT/mTOR pathway signatures were enhanced in HCV‐SVR‐DAA tumors. HCV‐SVR‐DAA was significantly associated with portal vein invasion ( p = 0.003) in comparison to HCV‐SVR‐IFN. Conclusion Our dataset potentially serves as a fundamental resource for the genomic characteristics of HCV‐SVR‐DAA tumors. Our comprehensive genetic profiling by WES revealed significant differences in the mutation rate of several driver genes between HCV‐positive tumors and HCV‐SVR tumors. Furthermore, it was revealed that the frequency of samples with mutations in TP53 was significantly higher in HCV‐SVR‐DAA tumors than in HCV‐SVR‐IFN tumors.

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“…[Tong et al [ 247 ] reviewed the biological mechanisms (especially DNA damage repair) mediated by SMARCAD1.] ARID2 (AT-rich Interactive Domain 2) genes also encode subunits of SWI/SNF remodellers, which is associated with hepatocellular carcinoma (see review by Loesch et al [ 248 ]).…”

Section: Key Structural Elements Mediating 3d Chromatin Interactionsmentioning

confidence: 99%

3D chromatin architecture and transcription regulation in cancer

2022

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Chromatin has distinct three-dimensional (3D) architectures important in key biological processes, such as cell cycle, replication, differentiation, and transcription regulation. In turn, aberrant 3D structures play a vital role in developing abnormalities and diseases such as cancer. This review discusses key 3D chromatin structures (topologically associating domain, lamina-associated domain, and enhancer–promoter interactions) and corresponding structural protein elements mediating 3D chromatin interactions [CCCTC-binding factor, polycomb group protein, cohesin, and Brother of the Regulator of Imprinted Sites (BORIS) protein] with a highlight of their associations with cancer. We also summarise the recent development of technologies and bioinformatics approaches to study the 3D chromatin interactions in gene expression regulation, including crosslinking and proximity ligation methods in the bulk cell population (ChIA-PET and HiChIP) or single-molecule resolution (ChIA-drop), and methods other than proximity ligation, such as GAM, SPRITE, and super-resolution microscopy techniques.

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ARID2 Chromatin Remodeler in Hepatocellular Carcinoma

Cited by 16 publications

References 79 publications

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

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

Hepatocellular carcinoma after a sustained virological response by direct‐acting antivirals harborsTP53inactivation

3D chromatin architecture and transcription regulation in cancer

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