Gene copy number analysis of granulin-epithelin precursor (GEP) and ATP-binding cassette subfamily F member 1 (ABCF1) in hepatocellular carcinoma

Abstract Background Hepatocellular carcinoma (HCC) is the most common type of liver cancer that occurs predominantly in patients with previous liver conditions. In the absence of an ideal screening modality, HCC is usually diagnosed at an advanced stage. Recent studies show that loss or gain of genomic materials can activate the oncogenes or inactivate the tumor suppressor genes to predispose cells toward carcinogenesis. Here, we evaluated both the copy number alteration (CNA) and RNA sequencing data of 361 HCC samples in order to locate the frequently altered chromosomal regions and identify the affected genes. Results Our data show that the chr1q and chr8p are two hotspot regions for genomic amplifications and deletions respectively. Among the amplified genes, YY1AP1 (chr1q22) possessed the largest correlation between CNA and gene expression. Moreover, it showed a positive correlation between CNA and tumor grade. Regarding deleted genes, CHMP7 (chr8p21.3) possessed the largest correlation between CNA and gene expression. Protein products of both genes interact with other cellular proteins to carry out various functional roles. These include ASH1L, ZNF496, YY1, ZMYM4, CHMP4A, CHMP5, CHMP2A and CHMP3, some of which are well-known cancer-related genes. Conclusions Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments.

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Candidate gene copy number analysis by PCR and multicapillary electrophoresis

Electrophoresis ◽

10.1002/elps.200800755 ◽

2009 ◽

Vol 30 (7) ◽

pp. 1098-1101 ◽

Cited By ~ 8

Author(s):

Eszter Szantai ◽

Zsuzsanna Elek ◽

András Guttman ◽

Maria Sasvari-Szekely

Keyword(s):

Candidate Gene ◽

Copy Number ◽

Gene Copy Number ◽

Gene Copy ◽

Copy Number Analysis

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MLGA a rapid and cost-efficient assay for gene copy-number analysis

Nucleic Acids Research ◽

10.1093/nar/gkm651 ◽

2007 ◽

Vol 35 (17) ◽

pp. e115-e115 ◽

Cited By ~ 19

Author(s):

M. Isaksson ◽

J. Stenberg ◽

F. Dahl ◽

A.-C. Thuresson ◽

M.-L. Bondeson ◽

...

Keyword(s):

Copy Number ◽

Gene Copy Number ◽

Gene Copy ◽

Copy Number Analysis ◽

Cost Efficient

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Epidermal growth factor receptor expression and gene copy number analysis in gastric carcinoma samples from Chinese patients

Oncology Letters ◽

10.3892/ol.2015.3875 ◽

2015 ◽

Vol 11 (1) ◽

pp. 173-181 ◽

Cited By ~ 3

Author(s):

FAN ZHANG ◽

XINGWU YANG ◽

LIANHONG LI ◽

LEI SUN ◽

BO WANG ◽

...

Keyword(s):

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Copy Number ◽

Gene Copy Number ◽

Growth Factor Receptor ◽

Receptor Expression ◽

Chinese Patients ◽

Gene Copy ◽

Copy Number Analysis ◽

Epidermal Growth

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Identification of factors regulating the gene expression of alcohol dehydrogenases in hepatocellular carcinoma

10.21203/rs.3.rs-810174/v1 ◽

2021 ◽

Author(s):

Jinghe Xie ◽

Yaqi Qiu ◽

Shuai Zhang ◽

Keqing Ma ◽

Yimeng Ou ◽

...

Keyword(s):

Gene Expression ◽

Hepatocellular Carcinoma ◽

Dna Methylation ◽

Copy Number ◽

Gene Copy Number ◽

Copy Number Variations ◽

The Cancer Genome Atlas ◽

Gene Copy ◽

Excessive Alcohol Consumption ◽

Alcohol Dehydrogenases

Abstract Background Excessive alcohol consumption has been documented to increase the risk of liver hepatocellular carcinoma (HCC) development. Accordingly, a broad interest pointed to alcohol dehydrogenases (ADHs), which display essential roles in alcohol metabolism. Despite the relevance of ADHs expression and the prognosis of HCC has been estimated, so far, limited research concerning the factors that are responsible for the regulation of ADHs expression has been reported. Methods In this study, using The Cancer Genome Atlas (TCGA) and RegNetwork database, we predicted potential factors consisting of DNA methylation, gene copy number variations, transcription factors (TFs) and microRNAs (miRNAs) that might impact ADHs gene expression in HCC. Results We found that DNA methylation induced the down-regulated expression of ADH1B. Of note, our results implicated that gene copy number variation might not have effects on ADHs expression. Regarding TFs, we speculated that NFYA modulated ADH1C, E2F1 and TFAP2A regulated ADH6 expression based on their expression and prognostic value. Moreover, miR-185 and miR-561 might elicit the repression of ADH4, and miR-105 might impair ADH6 expression. Conclusion This study revealed that multiple factors, including DNA methylation, TFs and microRNAs, affect the expression of ADH family members, which provided new insights into discovering promising HCC-suppressive targets.

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