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[G. Cell differentiation, division, and death-22]



                Identification of Novel Biomarker and Signaling pathways


               Associated with Interstitial Cystitis/Bladder Pain Syndrome


                                             for Better Diagnosis



          Subbroto Kumar Saha¹˙#, Tak Il Jeon¹˙#, Soo Bin Jang¹˙#, Yu Jin Choi¹, Se Jong Kim¹, Kyung Min Lim¹, Hee Jeong

              Kwak¹, Yoon Joo Lee¹, Jong Yub An¹, Han Bit Bong¹, Hyeong Gon Kim², A ram Kim²˙*, Ssang Goo Cho¹˙*


            ¹Stem Cell and Regenerative Biotechnology, Konkuk University, SEOUL 05029, 대한민국, ²Urology, Konkuk

                    University Medical Center, Konkuk University School of Medicine, SEOUL 05029, 대한민국




        The complexity of interstitial cystitis/bladder pain syndrome (IC/BPS) has led to considerable uncertainty in terms
        of diagnosis and prevalence of the condition. Here, we try to identify the IC/BPS-associated genes through an

        integrated analysis of Gene Expression Omnibus datasets and confirm experimentally to predict the pathologic
        diagnosis of IC/BPS. Data mining analysis of GEO datasets revealed a total of 53 common differentially expressed

        genes in IC/BPS. A protein–protein interaction network was then constructed with the 53 common DEGs using
        Cytoscape v3.7.2, and next, six hub genes (CD5, CD38, ITGAL, IL7R, KLRB1, and IL7R) were identified using cytoHubba

        v0.1 that were upregulated in IC/BPS. Enrichment analysis of common DEGs revealed that hematopoietic cell lineage,
        immune system, and T-cell receptor signaling in naïve CD4+ T cell signaling pathways were prominently involved

        with the common 51 upregulated DEGs. Moreover, our RT-PCR data confirmed that the expression of the five hub
        genes (CD38, ITGAL, IL7R, KLRB1, and IL7R) was significantly augmented in IC/BPS patients’ samples when compared

        with their normal  counterparts. In  this study,  we systematically  predict  the  significant  biomarkers  and  possible
        signaling pathways involved in IC/BPS.
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