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Downloaded 1018 Mrna Sequencing an Increasing Trend in Isocitrate Dehydrogenase 1(IDH1) and 301 Mrna Microarray Data from the CGGA Data- -Mutant Gliomas (Ohba Et Al Liu et al. Mol Med (2021) 27:52 https://doi.org/10.1186/s10020-021-00316-0 Molecular Medicine RESEARCH ARTICLE Open Access Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients Zhendong Liu1,3†, Wang Zhang2†, Xingbo Cheng2†, Hongbo Wang1, Lu Bian1, Jialin Wang1, Zhibin Han2, Yanbiao Wang1, Xiaoyu Lian1, Binfeng Liu1, Zhishuai Ren1, Bo Zhang1, Zhenfeng Jiang2, Zhiguo Lin2* and Yanzheng Gao1,3* Abstract Background: XRCC2, a homologous recombination-related gene, has been reported to be associated with a variety of cancers. However, its role in glioma has not been reported. This study aimed to fnd out the role of XRCC2 in glioma and reveal in which glioma-specifc biological processes is XRCC2 involved based on thousands of glioma samples, thereby, providing a new perspective in the treatment and prognostic evaluation of glioma. Methods: The expression characteristics of XRCC2 in thousands of glioma samples from CGGA and TCGA data- bases were comprehensively analyzed. Wilcox or Kruskal test was used to analyze the expression pattern of XRCC2 in gliomas with diferent clinical and molecular features. The efect of XRCC2 on the prognosis of glioma patients was explored by Kaplan–Meier and Cox regression. Gene set enrichment analysis (GSEA) revealed the possible cellular mechanisms involved in XRCC2 in glioma. Connectivity map (CMap) was used to screen small molecule drugs target- ing XRCC2 and the expression levels of XRCC2 were verifed in glioma cells and tissues by RT-qPCR and immunohisto- chemical staining. Results: We found the overexpression of XRCC2 in glioma. Moreover, the overexpressed XRCC2 was associated with a variety of clinical features related to prognosis. Cox and meta-analyses showed that XRCC2 is an independent risk factor for the poor prognosis of glioma. Furthermore, the results of GSEA indicated that overexpressed XRCC2 could promote malignant progression through involved signaling pathways, such as in the cell cycle. Finally, doxazosin, quinostatin, canavanine, and chrysin were identifed to exert anti-glioma efects by targeting XRCC2. Conclusions: This study analyzed the expression pattern of XRCC2 in gliomas and its relationship with prognosis using multiple datasets. This is the frst study to show that XRCC2, a novel oncogene, is signifcantly overexpressed in glioma and can lead to poor prognosis in glioma patients. XRCC2 could serve as a new biomarker for glioma diagno- sis, treatment, and prognosis evaluation, thus bringing new insight into the management of glioma. Keywords: Glioma, XRCC2, Oncogene, Prognosis, Biomarker *Correspondence: [email protected]; [email protected]. Background edu.cn †Zhendong Liu, Wang Zhang and Xingbo Cheng contributed equally to Glioma is the most common primary tumor among this work adult brain tumors and has high mortality and disability 1 Department of Orthopaedics, Henan Provincial People’s Hospital, rates (Tan 2020). Currently, the treatment of glioma is People’s Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, Henan, China mainly surgical intervention and postoperative adjuvant 2 Department of Neurosurgery, The First Afliate Hospital of Harbin chemoradiotherapy (Lim et al. 2018). Although there are Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, many new methods for treating glioma (Pulkkanen and China Full list of author information is available at the end of the article Yla-Herttuala 2005; Kamran 2018; Mahmoudi 2019), the © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. Liu et al. Mol Med (2021) 27:52 Page 2 of 15 prognosis of glioma patients remains unsatisfactory. Tar- role in its pathophysiology (Kleibl and Kristensen 2016; geted therapy attacking specifc genes within the tumor- Lin 2011). Previous studies have also shown that XRCC2 ous cells may provide new ways to kill glioma cells and is abnormally expressed in a variety of tumors, includ- improve the prognosis of patients. Terefore, it is vital to ing rectal and breast cancers, and that it participates in fnd new and efective molecular targets for the diagnosis many cell signaling pathways (Chen 2018; Andreassen and treatment of glioma. and Hanenberg 2019; Xu 2014; Bashir et al. 2014). In In recent years, research on molecular targeted ther- addition, XRCC1 has been reported as one of the possible apy has proliferated greatly, and genes related to glioma genes involved in glioma prognosis (Jiang 2013). How- diagnosis, treatment, and prognosis have been screened ever, the role and expression pattern of XRCC2 in glioma and identifed. For instance, the B-RAF proto-oncogene have not been elucidated so far. encoded protein has a regulatory role in the MAPK/ERK Currently, computational research has opened new signaling pathway, which regulates glioma cell division avenues for advanced research on cancer management. and diferentiation (Lassaletta 2017); KRAS mutations are Many recent reports have used in silico approaches to associated with malignant progression of glioma (Fiora- predict the potential role of numerous genes and proteins vanzo 2019); the zinc fnger E-box binding homeobox 1 in the development of diferent types of cancer (Andreas- can inhibit the transcription of interleukin-2 and inhibit sen and Hanenberg 2019; Khan et al. 2017; Li 2020). the invasion and epithelial-mesenchymal transition of Terefore, we attempted to clarify the expression pattern glioma cells (Siebzehnrubl 2013). Although these stud- of XRCC2 in glioma through a joint analysis of multiple ies have enriched the molecular pool related to glioma databases, to explore the correlation between the expres- diagnosis and treatment, the prognosis of glioma patients sion pattern of XRCC2 and the clinical and molecu- is yet to be signifcantly improved, which may be due to lar characteristics of glioma, and to reveal the value of the fact that the malignant progression of gliomas is trig- XRCC2 in the prognostic evaluation of glioma. Overall, gered by a variety of complex factors rather than by a sin- we aimed to identify a novel therapeutic target for glioma gle oncogene. Terefore, more genes need to be screened and to contribute to the enlargement of the molecular and identifed to enrich the molecular pool for glioma pool for glioma diagnosis and treatment. diagnosis and treatment, thus bringing hope for improv- ing the prognosis of glioma patients. Materials and methods Te malignant transformation of a normal cell is the Data collection result of multiple factors, among which DNA double- Gene Expression Profling Interactive Analysis 2 strand breaks (DSBs) are the most lethal form of cell (GEPIA2, http:// gepia2. cancer- pku. cn/) integrates RNA- damage (Ceccaldi et al. 2016; Hoppe et al. 2018; Frappart seq data from Te Cancer Genome Atlas (TCGA) and 2009). As one of the repair methods for DSBs, homolo- Genotype-Tissue Expression (GTEx) databases (Tang gous recombination plays an important role in main- et al. 2019; Consortium GT 2015). We used GEPIA2 to taining the stability of chromosomes and inhibiting the preliminarily explore the expression of XRCC2 in dif- infnite replication of cells; the dysfunction of this repair ferent cancers and their corresponding normal tissues, method can increase the risk of cancer (Hoppe et al. including 163 glioblastoma samples and 207 normal 2018; Chen 2018; Hallam et al. 2015). It is well known brain tissue samples. Since the database is an online that RAD51, a DNA repair protein, plays a central role in analysis platform, the expression level of XRCC2 in dif- regulating the homologous recombination repair process ferent tumors can be obtained by inputting XRCC2 in the of DSBs (Shen 2018; Cruz 2018). Moreover, studies have search page. shown that after ionizing radiation exposure, RAD51 Te Chinese Glioma Genome Atlas (CGGA, http:// participates in cell cycle changes in glioblastoma stem www. cgga. org. cn/) database contains thousands of gli- cells (Tachon 2018). Furthermore, Ohba et al. found that oma gene expression data and the corresponding clinical RAD51-mediated homologous recombination showed information. We downloaded 1018 mRNA sequencing an increasing trend in isocitrate dehydrogenase 1(IDH1) and 301 mRNA microarray data from the CGGA data- -mutant gliomas (Ohba et al. 2014). XRCC2, a homolo- base, of which the mRNA sequencing and mRNA micro- gous gene of RAD51, can form a complex with three array data with complete clinical information were 748 RAD51 paralogs (RAD51B, RAD51C, and RAD51D), and and 268, respectively. Te original data in the database it participates in homologous recombination by encod- has been standardized, so after downloading the origi- ing members of
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