Gene co-expression analysis applied to RNASEH2A reveals functional networks associated with DNA replication, DNA damage response, as well as cell cycle regulation

2020 ◽  
Author(s):  
Stefania Marsili
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Expression Analysis ◽  
Cell Cycle Regulation ◽  
Functional Networks ◽  
Damage Response ◽  
Cycle Regulation

scholarly journals Gene co-expression analysis of human RNASEH2A reveals functional networks associated with DNA replication, DNA damage response, and cell cycle regulation

2020 ◽  
Author(s):  
Stefania Marsili ◽  
Ailone Tichon ◽  
Francesca Storici
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Functional Networks ◽  
Biological Processes ◽  
Damage Response ◽  
Rnase H2 ◽  
Cycle Regulation

AbstractRibonuclease H2 (RNase H2) is a key enzyme for the removal of RNA found in DNA-RNA hybrids, playing a fundamental role in biological processes such as DNA replication, telomere maintenance and DNA damage repair. RNase H2 is a trimer composed of three subunits, being RNASEH2A the catalytic subunit. RNASEH2A expression levels have been shown to be upregulated in transformed and cancer cells. In this study we used a bioinformatics approach to identify RNASEH2A co-expressed genes in different human tissues to uncover biological processes in which RNASEH2A is involved. By implementing this approach, we identified functional networks for RNASEH2A that are not only involved in the processes of DNA replication and DNA damage response, but also in cell cycle regulation. Additional examination of protein-protein networks for RNASEH2A by the STRING database analysis, revealed a high co-expression correlation between RNASEH2A and the genes of the protein networks identified. Mass spectrometry analysis of RNASEH2A-bound proteins highlighted players functioning in cell cycle regulation. Further bioinformatics investigation showed increased gene expression of RNASEH2A in different types of actively cycling cells and tissues, and particularly in several cancers, supporting a biological role for RNASEH2A, but not the other two subunits of RNase H2, in cell proliferation.

scholarly journals Gene Co-Expression Analysis of Human RNASEH2A Reveals Functional Networks Associated with DNA Replication, DNA Damage Response, and Cell Cycle Regulation

Biology ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 221
Author(s):  
Stefania Marsili ◽  
Ailone Tichon ◽  
Deepali Kundnani ◽  
Francesca Storici
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Functional Networks ◽  
Biological Processes ◽  
Damage Response ◽  
Rnase H2 ◽  
Cycle Regulation

Ribonuclease (RNase) H2 is a key enzyme for the removal of RNA found in DNA-RNA hybrids, playing a fundamental role in biological processes such as DNA replication, telomere maintenance, and DNA damage repair. RNase H2 is a trimer composed of three subunits, RNASEH2A being the catalytic subunit. RNASEH2A expression levels have been shown to be upregulated in transformed and cancer cells. In this study, we used a bioinformatics approach to identify RNASEH2A co-expressed genes in different human tissues to underscore biological processes associated with RNASEH2A expression. Our analysis shows functional networks for RNASEH2A involvement such as DNA replication and DNA damage response and a novel putative functional network of cell cycle regulation. Further bioinformatics investigation showed increased gene expression in different types of actively cycling cells and tissues, particularly in several cancers, supporting a biological role for RNASEH2A but not for the other two subunits of RNase H2 in cell proliferation. Mass spectrometry analysis of RNASEH2A-bound proteins identified players functioning in cell cycle regulation. Additional bioinformatic analysis showed that RNASEH2A correlates with cancer progression and cell cycle related genes in Cancer Cell Line Encyclopedia (CCLE) and The Cancer Genome Atlas (TCGA) Pan Cancer datasets and supported our mass spectrometry findings.

scholarly journals Role of the Polymerase ϵ sub-unit DPB2 in DNA replication, cell cycle regulation and DNA damage response in Arabidopsis

2016 ◽  
pp. gkw449 ◽  
Author(s):  
José Antonio Pedroza-Garcia ◽  
Séverine Domenichini ◽  
Christelle Mazubert ◽  
Mickael Bourge ◽  
Charles White ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Damage Response ◽  
Cycle Regulation

scholarly journals PCNA-Mediated Degradation of p21 Coordinates the DNA Damage Response and Cell Cycle Regulation in Individual Cells

Cell Reports ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 48-58.e7 ◽  
Author(s):  
Caibin Sheng ◽  
Isabella-Hilda Mendler ◽  
Sara Rieke ◽  
Petra Snyder ◽  
Marcel Jentsch ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Damage Response ◽  
Cycle Regulation

SP-02: Cell Cycle Regulation of the DNA Damage Response: Targeting WEE1 Kinase to Impair DNA Repair.

2012 ◽  
Vol 104 ◽  
pp. 21
Author(s):  
M.A.T.M. Van Vugt ◽  
M. Krajewska ◽  
H. Sillje ◽  
A.M. Heijink ◽  
Y. Bisselink ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Damage Response ◽  
Wee1 Kinase ◽  
Cycle Regulation

scholarly journals NFBD1/MDC1: DNA damage response, cell cycle regulation and carcinogenesis

2015 ◽  
Vol 1 (1) ◽  
pp. 49-59 ◽  
Author(s):  
Toshinori Ozaki ◽  
◽  
Youquan Bu ◽  
Hiroki Nagase ◽  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Damage Response ◽  
Cycle Regulation

scholarly journals Cell Cycle Regulation and DNA Damage Response Networks in Diffuse- and Intestinal-Type Gastric Cancer

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5786
Author(s):  
Shihori Tanabe ◽  
Sabina Quader ◽  
Ryuichi Ono ◽  
Horacio Cabral ◽  
Kazuhiko Aoyagi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Intestinal Type ◽  
Diffuse Type ◽  
Damage Response ◽  
Canonical Pathways ◽  
Cycle Regulation

Dynamic regulation in molecular networks including cell cycle regulation and DNA damage response play an important role in cancer. To reveal the feature of cancer malignancy, gene expression and network regulation were profiled in diffuse- and intestinal-type gastric cancer (GC). The results of the network analysis with Ingenuity Pathway Analysis (IPA) showed that the activation states of several canonical pathways related to cell cycle regulation were altered. The G1/S checkpoint regulation pathway was activated in diffuse-type GC compared to intestinal-type GC, while canonical pathways of the cell cycle control of chromosomal replication, and the cyclin and cell cycle regulation, were activated in intestinal-type GC compared to diffuse-type GC. A canonical pathway on the role of BRCA1 in the DNA damage response was activated in intestinal-type GC compared to diffuse-type GC, where gene expression of BRCA1, which is related to G1/S phase transition, was upregulated in intestinal-type GC compared to diffuse-type GC. Several microRNAs (miRNAs), such as mir-10, mir-17, mir-19, mir-194, mir-224, mir-25, mir-34, mir-451 and mir-605, were identified to have direct relationships in the G1/S cell cycle checkpoint regulation pathway. Additionally, cell cycle regulation may be altered in epithelial-mesenchymal transition (EMT) conditions. The alterations in the activation states of the pathways related to cell cycle regulation in diffuse- and intestinal-type GC highlighted the significance of cell cycle regulation in EMT.

scholarly journals Cell Cycle Regulation and DNA Damage Response Networks in Diffuse-and Intestinal-Type Gastric Cancer

2021 ◽  
Author(s):  
Shihori Tanabe ◽  
Sabina Quader ◽  
Ryuichi Ono ◽  
Horacio Cabral ◽  
Kazuhiko Aoyagi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Intestinal Type ◽  
Diffuse Type ◽  
Damage Response ◽  
Canonical Pathways ◽  
Cycle Regulation

Epithelial-mesenchymal transition (EMT) networks are essential in acquiring the drug resistance and cancer malignant features in cancer stem cells (CSCs). In this regard, gene expression profiles in diffuse- and intestinal-type gastric cancer (GC) have been analyzed to reveal the network pathways in EMT and CSCs, since the diffuse-type GC has much more mesenchymal features than intestinal-type GC that has the intestinal features. The study results revealed that the activation state of several canonical pathways related to cell cycle regulation was altered. The canonical pathway on Cell cycle: G1/S checkpoint regulation was activated in diffuse-type GC, and canonical pathways on Cell cycle control of chromosomal replication and Cyclins and cell cycle regulation were activated in intestinal-type GC. Canonical pathway related to Role of BRCA1 in DNA damage response was activated in intestinal-type GC, where BRCA1, which is related to G1/S phase transition was up-regulated in intestinal-type GC. Several microRNAs (miRNAs), including mir-10, mir-17, mir-19, mir-194, mir-224, mir-25, mir-34, mir-451, and mir-605, were identified to have direct relationships of RNA-RNA interaction in Cell cycle: G1/S checkpoint regulation pathway. Additionally, cell cycle regulation may be altered in EMT conditions. The alterations in activation states of the pathways related to cell cycle regulation in diffuse- and intestinal-type GC would indicate the significance of cell cycle regulation in EMT.

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