title: Aberrant methylation profile of 14-3-3 sigma and its reduced transcription/expression levels in Chinese sporadic female breast carcinogenesis.
abstract: To study the relation of 14-3-3 sigma gene promoter hypermethylation and its transcription expression levels in sporadic breast carcinogenesis. Methylation of 14-3-3 sigma gene was detected by sensitive MSP assay in carcinous, non-cancerous, and normal tissue, and its mRNA was also detected by real time PCR based on SYBR Green 1 as well, and protein was detected by west blotting assay. The methylation frequencies of 14-3-3 sigma were 90% in 68 cases of sporadic breast cancer patients. Methylation was presented in portions (2/13, 18%) of hyperplastic samples, and no hypermethylation was presented in normal tissue. The methylation change of 14-3-3 sigma gene was markedly related with various types, grades, and lymph node metastases (P < 0.05), and no significant differences in methylation frequencies were seen between premenopause and postmenopause (P > 0.05). The methylation of 14-3-3 sigma shows reverse relation with its mRNA transcription and expression level (P < 0.05). Only was lymph node metastases strongly associated with poor outcome (P = 0.02). Whether 14-3-3 sigma promoter methylation or not did not affect the 5 years survival rate of sporadic breast cancer patients (P > 0.05). Epigenetics alterations of the 14-3-3 sigma can contribute to reducing or losing expression of 14-3-3 sigma protein, which play an important role in the development of sporadic breast carcinomas and involved in various types, grades, and lymph node metastases. Otherwise, node metastases of breast carcinogenesis patients are strongly associated with poor outcome.
authors.affiliation: The Neurosurgery Department, Taihe Hospital, Yunyang Medicinal College, Shiyan, Hubei, 442000, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Luo
authors.forename: Jing
authors.initials: J
authors.lastname: Feng
authors.forename: Jun
authors.initials: J
authors.lastname: Lu
authors.forename: Yuping
authors.initials: Y
authors.lastname: Wang
authors.forename: Xuanbin
authors.initials: X
authors.lastname: Tang
authors.forename: Fei
authors.initials: F
authors.lastname: Xie
authors.forename: Wenbin
authors.initials: W
authors.lastname: Li
mesh_terms: D048948:14-3-3 Proteins / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology; D000328:Adult; D000368:Aged; D014408:Biomarkers, Tumor / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology; D001943:Breast Neoplasms / Q000737:chemistry / Q000208:ethnology / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002277:Carcinoma / Q000737:chemistry / Q000208:ethnology / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D002681:China / Q000453:epidemiology; D018899:CpG Islands / Q000235:genetics*; D019175:DNA Methylation; D004273:DNA, Neoplasm / Q000032:analysis*; D004847:Epithelial Cells / Q000378:metabolism; D005092:Exonucleases / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology; D005095:Exoribonucleases; D005260:Female; D005348:Fibrocystic Breast Disease / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D020868:Gene Silencing; D006801:Humans; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis; D012334:RNA, Neoplasm / Q000096:biosynthesis
chemical_list: D048948:14-3-3 Proteins; D014408:Biomarkers, Tumor; D004273:DNA, Neoplasm; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D005092:Exonucleases; D005095:Exoribonucleases; C413442:SFN protein, human
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