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Biosystem analysis of the hypoxia inducible domain family member 2A: Implications in cancer biology

dc.contributor.authorSalazar C.
dc.contributor.authorYañez O.
dc.contributor.authorElorza A.A.
dc.contributor.authorCortes N.
dc.contributor.authorGarcía-Beltrán O.
dc.contributor.authorTiznado W.
dc.contributor.authorRuiz L.M.
dc.date.accessioned2020-09-02T22:27:39Z
dc.date.available2020-09-02T22:27:39Z
dc.date.issued2020
dc.identifier10.3390/genes11020206
dc.identifier.citation11, 2, -
dc.identifier.issn20734425
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6152
dc.descriptionThe expression of HIGD2A is dependent on oxygen levels, glucose concentration, and cell cycle progression. This gene encodes for protein HIG2A, found in mitochondria and the nucleus, promoting cell survival in hypoxic conditions. The genomic location of HIGD2A is in chromosome 5q35.2, where several chromosomal abnormalities are related to numerous cancers. The analysis of high definition expression profiles of HIGD2A suggests a role for HIG2A in cancer biology. Accordingly, the research objective was to perform a molecular biosystem analysis of HIGD2A aiming to discover HIG2A implications in cancer biology. For this purpose, public databases such as SWISS-MODEL protein structure homology-modelling server, Catalogue of Somatic Mutations in Cancer (COSMIC), Gene Expression Omnibus (GEO), MethHC: a database of DNA methylation and gene expression in human cancer, and microRNA-target interactions database (miRTarBase) were accessed. We also evaluated, by using Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR), the expression of Higd2a gene in healthy bone marrow-liver-spleen tissues of mice after quercetin (50 mg/kg) treatment. Thus, among the structural features of HIG2A protein that may participate in HIG2A translocation to the nucleus are an importin α-dependent nuclear localization signal (NLS), a motif of DNA binding residues and a probable SUMOylating residue. HIGD2A gene is not implicated in cancer via mutation. In addition, DNA methylation and mRNA expression of HIGD2A gene present significant alterations in several cancers; HIGD2A gene showed significant higher expression in Diffuse Large B-cell Lymphoma (DLBCL). Hypoxic tissues characterize the “bone marrow-liver-spleen” DLBCL type. The relative quantification, by using RT-qPCR, showed that Higd2a expression is higher in bone marrow than in the liver or spleen. In addition, it was observed that quercetin modulated the expression of Higd2a gene in mice. As an assembly factor of mitochondrial respirasomes, HIG2A might be unexpectedly involved in the change of cellular energetics happening in cancer. As a result, it is worth continuing to explore the role of HIGD2A in cancer biology. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectCancer
dc.subjectDNA methylation
dc.subjectHIGD2A
dc.subjectHypoxia
dc.subjectMiRNA
dc.subjectMRNA expression
dc.subjectQuercetin
dc.subjectDNA
dc.subjecthypoxia inducible domain family member 2A
dc.subjecthypoxia inducible factor
dc.subjectmicroRNA
dc.subjectquercetin
dc.subjectunclassified drug
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbone marrow
dc.subjectcell energy
dc.subjectcell nucleus
dc.subjectcontrolled study
dc.subjectdiffuse large B cell lymphoma
dc.subjectDNA binding
dc.subjectDNA methylation
dc.subjectembryo
dc.subjectgene
dc.subjectgene expression
dc.subjectHIGD2A gene
dc.subjecthuman
dc.subjecthuman cell
dc.subjectinfant
dc.subjectliver
dc.subjectmale
dc.subjectmalignant neoplasm
dc.subjectmitochondrial respiration
dc.subjectmouse
dc.subjectnonhuman
dc.subjectnuclear localization signal
dc.subjectpathogenesis
dc.subjectprotein assembly
dc.subjectprotein motif
dc.subjectprotein structure
dc.subjectprotein transport
dc.subjectsomatic mutation
dc.subjectspleen
dc.subjectsumoylation
dc.titleBiosystem analysis of the hypoxia inducible domain family member 2A: Implications in cancer biology
dc.typeArticle


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