基于GEO数据库探索成釉细胞瘤与牙源性角化囊肿间差异基因

Abstract

Abstract: Objective　To find the differential expression genes (DEGs) between ameloblastoma and odontogenic keratocyst, analyze their function, and explore the mechanism of ameloblastoma invasion and growth. Methods The gene chip data set GSE38494 was downloaded from GEO database. The LIMMA packets was used to analyze the differential expression genes between ameloblastoma and odontogenic keratocyst. Then the Database for Annotation, Visualization and Integrated Discovery (DIVID) was employed to analyze Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The PPI network of differential expression genes was constructed on Search Tool for the Retrieval of Interacting Genes (STRING) website. The results were visualized by Cytoscape software, and the hub genes were screened by MCODE plug-in. Results 335 differential genes were identified. GO analysis showed that differential genes mainly affected neuronal differentiation, cell adhesion, biological adhesion, cell morphogenesis involved in differentiation, cell fate commitment and other biological processes. Cell component enrichment was mainly involved in extracellular domain, extracellular matrix, extracellular region, proteinaceous extracellular matrix, component and synapse of extracellular matrix structure and so on. The molecular function of enrichment was mainly involved in carbohydrate binding, heparin binding and transcription factor activity. KEGG pathway analysis showed that differential genes were mainly engaged in signaling pathways such as ECM-receptor interaction, axon orientation and pathway in cancer. The 8 hub genes were SPARCL1, SERPINA1, ITIH2, IGFBP5, LAMB1, C3, GOLM1 and FAM20A. Conclusion The DEGs between ameloblastoma and odontogenic keratocyst are screened out by means of bioinformatics. The 8 hub genes are expected to become new markers for differential diagnosis between ameloblastoma and odontogenic keratocyst, and provide new ideas for studies on ameloblastoma.

Key words: GEO database, ameloblastoma, odontogenic keratocyst, differential expression genes, bioinformatics analysis

CLC Number:

R739.82

References 39

	［参　考　文　献］
[1]	El-Naggar A, Chan J, Grandis J, et al. WHO classification of head and neck tumours [M]. International Agency for Research on Cancer, 2017.
[2]	Effiom O A, Ogundana O M, Akinshipo A O, et al. Ameloblastoma: current etiopathological concepts and management[J]. Oral Dis, 2018,24(3):307~316.
[3]	Speight P M, Takata T. New tumour entities in the 4th edition of the World Health Organization Classification of Head and Neck tumours: odontogenic and maxillofacial bone tumours[J]. Virchows Arch, 2018,472(3):331~339.
[4]	Chrcanovic B R, Gomez R S. Recurrence probability for keratocystic odontogenic tumors: An analysis of 6427 cases[J]. J Craniomaxillofac Surg, 2017,45(2):244~251.
[5]	王彦瑾，谢晓艳，洪瑛瑛，等. 844例牙源性角化囊肿的临床病理学分析[J]. 北京大学学报(医学版), 2019:1~18.
[6]	陶谦，梁培盛. 2017版WHO牙源性肿瘤新分类之述评[J]. 口腔疾病防治, 2017(12):749~754.
[7]	Sweeney R T, Mcclary A C, Myers B R, et al. Identification of recurrent SMO and BRAF mutations in ameloblastomas[J]. Nat Genet, 2014,46(7):722~725.
[8]	Kaye F J, Ivey A M, Drane W E, et al. Clinical and radiographic response with combined BRAF-targeted therapy in stage 4 ameloblastoma[J]. J Natl Cancer Inst, 2015,107(1):378.
[9]	Pan S, Dong Q, Sun LS, et al. Mechanisms of Inactivation of PTCH1 Gene in Nevoid Basal Cell Carcinoma Syndrome: Modification of the Two-Hit Hypothesis[J]. Clin Cancer Res, 2010,16(2):442~450.
[10]	Liu J, Li R, Liao X, et al. Comprehensive Bioinformatic Analysis Genes Associated to the Prognosis of Liposarcoma[J]. Med Sci Monit, 2018,24:7329~7339.
[11]	Han B, Feng D, Yu X, et al. Identification and Interaction Analysis of Molecular Markers in Colorectal Cancer by Integrated Bioinformatics Analysis[J]. Med Sci Monit, 2018,24:6059~6069.
[12]	Heikinheimo K, Kurppa K J, Laiho A, et al. Early dental epithelial transcription factors distinguish ameloblastoma from keratocystic odontogenic tumor[J]. J Dent Res, 2015,94(1):101~111.
[13]	Ritchie M E, Phipson B, Wu D, et al. limma powers differential expression analyses for RNA-sequencing and microarray studies[J]. Nucleic Acids Res, 2015,43(7):e47.
[14]	Huang D W, Sherman B T, Lempicki R A. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources[J]. Nat Protoc, 2009,4(1):44~57.
[15]	Szklarczyk D, Franceschini A, Wyder S, et al. STRING v10: protein-protein interaction networks, integrated over the tree of life[J]. Nucleic Acids Res, 2015,43(Database issue):D447~D452.
[16]	Su G, Morris J H, Demchak B, et al. Biological network exploration with Cytoscape 3[J]. Curr Protoc Bioinformatics, 2014,47:8~13.
[17]	Wang J H, Zhao L F, Lin P, et al. GenCLiP 2.0: a web server for functional clustering of genes and construction of molecular networks based on free terms[J]. Bioinformatics, 2014,30(17):2534~2536.
[18]	Rozario T, Desimone D W. The extracellular matrix in development and morphogenesis: a dynamic view[J]. Dev Biol, 2010,341(1):126~140.
[19]	Gouirand V, Guillaumond F, Vasseur S. Influence of the Tumor Microenvironment on Cancer Cells Metabolic Reprogramming[J]. Front Oncol, 2018,8:117.
[20]	Wang M, Zhao J, Zhang L, et al. Role of tumor microenvironment in tumorigenesis[J]. J Cancer, 2017,8(5):761~773.
[21]	Peyton S R, Ghajar C M, Khatiwala C B, et al. The emergence of ECM mechanics and cytoskeletal tension as important regulators of cell function[J]. Cell Biochem Biophys, 2007,47(2):300~320.
[22]	陈志雷，王振军. 细胞外基质弹性纤维与普外科疾病[J]. 临床外科杂志,2018,26(06):472~473.
[23]	Fleming J M, Yeyeodu S T, Mclaughlin A, et al. In Situ Drug Delivery to Breast Cancer-Associated Extracellular Matrix[J]. ACS Chem Biol, 2018,13(10):2825~2840.
[24]	Pang J H, Coupland L A, Freeman C, et al. Activation of tumour cell ECM degradation by thrombin-activated platelet membranes: potentially a P-selectin and GPIIb/IIIa-dependent process[J]. Clin Exp Metastasis, 2015,32(5):495~505.
[25]	钱永，黄洪章，潘朝斌，等. RANKL、MMP-9和MMP-2在成釉细胞瘤中的表达及意义[J]. 中国口腔颌面外科杂志,2008(05):362~367.
[26]	Bradshaw A D. Diverse biological functions of the SPARC family of proteins[J]. Int J Biochem Cell Biol, 2012,44(3):480~488.
[27]	Turtoi A, Musmeci D, Naccarato A G, et al. Sparc-like protein 1 is a new marker of human glioma progression[J]. J Proteome Res, 2012,11(10):5011~5021.
[28]	Cao F, Wang K, Zhu R, et al. Clinicopathological significance of reduced SPARCL1 expression in human breast cancer[J]. Asian Pac J Cancer Prev, 2013,14(1):195~200.
[29]	Normandin K, Peant B, Le Page C, et al. Protease inhibitor SERPINA1 expression in epithelial ovarian cancer[J]. Clin Exp Metastasis, 2010,27(1):55~69.
[30]	Kloth J N, Gorter A, Fleuren G J, et al. Elevated expression of SerpinA1 and SerpinA3 in HLA-positive cervical carcinoma[J]. J Pathol, 2008,215(3):222~230.
[31]	Hamm A, Veeck J, Bektas N, et al. Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis[J]. BMC Cancer, 2008,8:25.
[32]	Pollak M. The insulin and insulin-like growth factor receptor family in neoplasia: an update[J]. Nat Rev Cancer, 2012,12(3):159~169.
[33]	Petz M, Them N C, Huber H, et al. PDGF enhances IRES-mediated translation of Laminin B1 by cytoplasmic accumulation of La during epithelial to mesenchymal transition[J]. Nucleic Acids Res, 2012,40(19):9738~9749.
[34]	Petz M, Them N, Huber H, et al. La enhances IRES-mediated translation of laminin B1 during malignant epithelial to mesenchymal transition[J]. Nucleic Acids Res, 2012,40(1):290~302.
[35]	Boire A, Zou Y, Shieh J, et al. Complement Component 3 Adapts the Cerebrospinal Fluid for Leptomeningeal Metastasis[J]. Cell, 2017,168(6):1101~1113.
[36]	张金彦，张帆，黄涛，等. 原发性肝癌患者血清补体C3水平的临床检测意义[J]. 浙江临床医学,2015(6):861~862.
[37]	Kim H J, Lv D, Zhang Y, et al. Golgi phosphoprotein 2 in physiology and in diseases[J]. Cell Biosci, 2012,2(1):31.
[38]	Varambally S, Laxman B, Mehra R, et al. Golgi protein GOLM1 is a tissue and urine biomarker of prostate cancer[J]. Neoplasia, 2008,10(11):1285~1294.
[39]	Kantaputra P N, Kaewgahya M, Khemaleelakul U, et al. Enamel-renal-gingival syndrome and FAM20A mutations[J]. Am J Med Genet A, 2014,164A(1):1~9.

Exploration of differential expression genes between ameloblastoma and odontogenic keratocyst based on GEO database

PDF (PC)

Knowledge

Abstract

Cite this article

share this article

References 39

Related Articles 2

Recommended Articles

Metrics

Comments

[1]	. Expression and significance of E-cadherin and vimentin in ameloblastoma and odontogenic cyst [J]. , 2018, 38(4): 300-304.
[2]	. Comparative study on the CBCT image of the mandibular ameloblastoma and keratocystic odontogenic tumor [J]. , 2018, 38(4): 320-323.