دورية أكاديمية
أعرض في EDS

miR-31 is consistently inactivated in EBV-associated nasopharyngeal carcinoma and contributes to its tumorigenesis.

التفاصيل البيبلوغرافية
العنوان: miR-31 is consistently inactivated in EBV-associated nasopharyngeal carcinoma and contributes to its tumorigenesis.
المؤلفون: Cheung CC, Chung GT, Lun SW, To KF, Choy KW, Lau KM, Siu SP, Guan XY, Ngan RK, Yip TT, Busson P, Tsao SW, Lo KW; Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People's Republic of China. kwlo@cuhk.edu.hk.
المصدر: Molecular cancer [Mol Cancer] 2014 Aug 07; Vol. 13, pp. 184. Date of Electronic Publication: 2014 Aug 07.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101147698 Publication Model: Electronic Cited Medium: Internet ISSN: 1476-4598 (Electronic) Linking ISSN: 14764598 NLM ISO Abbreviation: Mol Cancer Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, c2002-
مواضيع طبية MeSH: Carcinogenesis/*pathology , Herpesvirus 4, Human/*physiology , MicroRNAs/*metabolism , Nasopharyngeal Neoplasms/*genetics , Nasopharyngeal Neoplasms/*virology, Carcinogenesis/genetics ; Carcinoma ; Cell Movement/genetics ; Cell Proliferation ; Cell Survival/genetics ; Comparative Genomic Hybridization ; DNA Methylation/genetics ; Down-Regulation/genetics ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Homozygote ; Humans ; MicroRNAs/genetics ; Minichromosome Maintenance Complex Component 2/metabolism ; Mixed Function Oxygenases/metabolism ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms/pathology ; Phosphorylation ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Tumor Suppressor Protein p53/metabolism
مستخلص: Background: As a distinctive type of head and neck cancers, nasopharyngeal carcinoma (NPC) is genesis from the clonal Epstein-Barr virus (EBV)-infected nasopharyngeal epithelial cells accumulated with multiple genetic lesions. Among the recurrent genetic alterations defined, loss of 9p21.3 is the most frequent early event in the tumorigenesis of EBV-associated NPC. In addition to the reported CDKN2A/p16, herein, we elucidated the role of a miRNA, miR-31 within this 9p21.3 region as NPC-associated tumor suppressor.
Methods: The expression and promoter methylation of miR-31 were assessed in a panel of NPC tumor lines and primary tumors. Its in vitro and in vivo tumor suppression function was investigated through the ectopic expression of miR-31 in NPC cells. We also determined the miR-31 targeted genes and its involvement in the growth in NPC.
Results: Downregulation of miR-31 expression was detected in almost all NPC cell line, patient-derived xenografts (PDXs) and primary tumors. Both homozygous deletion and promoter hypermethylation were shown to be major mechanisms for miR-31 silencing in this cancer. Strikingly, loss of miR-31 was also obviously observed in the dysplastic lesions of nasopharynx. Restoration of miR-31 in C666-1 cells inhibited the cell proliferation, colony-forming and migratory capacities. Dramatic reduction of in vitro anchorage-independent growth and in vivo tumorigenic potential were demonstrated in the stable clones expressing miR-31. Furthermore, we proved that miR-31 suppressed the NPC cell growth via targeting FIH1 and MCM2.
Conclusions: The findings provide strong evidence to support miR-31 as a new NPC-associated tumor suppressor on 9p21.3 region. The inactivation of miR-31 may contribute to the early development of NPC.
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المشرفين على المادة: 0 (MIRN31 microRNA, human)
0 (MicroRNAs)
0 (Repressor Proteins)
0 (Tumor Suppressor Protein p53)
EC 1.- (Mixed Function Oxygenases)
EC 1.14.11.- (HIF1AN protein, human)
EC 3.6.4.12 (MCM2 protein, human)
EC 3.6.4.12 (Minichromosome Maintenance Complex Component 2)
تواريخ الأحداث: Date Created: 20140808 Date Completed: 20150702 Latest Revision: 20220321
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4127521
DOI: 10.1186/1476-4598-13-184
PMID: 25098679
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4598
DOI:10.1186/1476-4598-13-184