LILRB5, has-miR-22-3p, H19,MALAT1 ceRNA axis influences Kaposi Sarcoma cancer development by supervising “ Immune regulatory interactions between a Lymphoid and non-Lymphoid cell pathway” bioinformatics gene expression profiling and RNA interaction analyses.
LILRB5, has-miR-22-3p, H19,MALAT1 ceRNA axis influences Kaposi Sarcoma cancer development by supervising “ Immune regulatory interactions between a Lymphoid and non-Lymphoid cell pathway” bioinformatics gene expression profiling and RNA interaction analyses.
Fateme Moradi,1Marzie Heydari,2Mohammad Rezaei,3Mansoureh Azadeh,4,*
1. Zist fanavari Novin Biotechnology Institute, Isfahan, Iran 2. Zist fanavari Novin Biotechnology Institute, Isfahan, Iran 3. Zist fanavari Novin Biotechnology Institute, Isfahan, Iran 4. Zist fanavari Novin Biotechnology Institute, Isfahan, Iran
Introduction: Kaposi sarcoma (KS) is a low-grade vascular tumor associated with Kaposi sarcoma Herpes virus/Human herpes virus 8 (KSHV/HHV8) infection is the etiologic agent underlying Kaposi sarcoma[1]. Kaposi sarcoma lesions predominantly present at mucocutaneous sites, primary effusion lymphoma, and multicentric Castleman’s disease but may involve all organs and anatomic locations. This human gamma herpesvirus was discovered in 1994 by Drs. Yuan Chang and Patrick Moore. Today, there are over five thousand publications on KSHV and its associated malignancies[2]. In this investigate we concentrate on recent expression profiling by array about the genome-wide localization of the Kaposi sarcoma-associated Herpes virus and Murine gamma Herpes virus to find a gene with differentially expressed gene (DEG)that regulated to Kaposi sarcoma and find ceRNA and protein interaction.
Methods: Initially database GSE153601 were acquire NCBI Gene Expression Omnibus GEO and then analyzed byGEO2r to find differentially expressed genes and validation of expression analyses performed by GEPIA2 and ENCORI databases. Through GeneCard and ENrichr gene ontology information and biological pathway involvement were understood .Furthermore , Mirwalk was utilized to find significant miRNA-mRNA interactions.And selected miRNA was searched in Lncbase V.3 to find strong interactions with LncRNAs and contrust a predictive ceRNA network.
Results: eventually the LILRB5gene was selected for further exploration[3] .( log FC<0) (adj.p<.05) . Based on microarray analysis LILRB5is significantly reduction expression host chromatin Gepia2 and Encori[4] [5]. Gene ontology and pathway analysis were accomplished by the Enrichr database to strength association of the LILRB5[6] .Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell. A number of receptors and cell adhesion molecules play a key role in modifying the response of cells of lymphoid origin (such as B-, T- and NK cells) to self and tumor antigens, as well as to pathogenic organisms [7] [8]. Survey of miRNA and mRNA interactions (mir walk v.3) exhibit has-miR-22-3p to be a novel repressor for our gene [score=1] [9]. We searched possible lncRNA–mRNA interactions using(LncBase) and select H19 , MALAT1 which taken to gene card for lncRNA verification and also we analyzed miRNA -lncRNA interaction by(LncBase)[10].
Conclusion: We announced that has-miR-22-3p has significant interaction with MALAT1and H19 and may be these are ceRNA along for LILRB5 gene[11]. Eventually the mentioned lncRNA (MALAT1and H19) may act as transcriptional regulators for enormous gene.