High DRC Levels Are Associated with Let-7b Overexpression in Women with Breast CancerReportar como inadecuado




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1

Department of Basic Sciences, Division of Pharmacology and Toxicology, Ponce Research Institute, Ponce Health Sciences University-School of Medicine, Ponce, PR 00716-2347, Puerto Rico

2

Biology Department, University of Puerto Rico at Ponce, Ponce, PR 00716-9996, Puerto Rico

3

Department of Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA





*

Author to whom correspondence should be addressed.



Academic Editor: Guillermo T. Sáez

Abstract Nucleotide Excision Repair NER is a critical pathway involved in breast cancer BC. We have previously published that a low DNA repair capacity DRC is associated with a higher risk of BC in Puerto Rican women. Let-7b belongs to a miRNA family with tumor suppressor activity that targets oncogenes. We isolated miRNAs from plasma of 153 Puerto Rican women with and without BC. DRC was measured in lymphocytes by means of a host cell reactivation assay. These women were divided into four groups according to their DRC level: High >3.8% and low <3.8%. The four groups consisted of BC patients with high n = 35 and low n = 43 DRC and controls with high n = 39 and low n = 36 DRC. Epidemiologic data were collected at initial BC diagnosis and almost five years after diagnosis. A significant difference in Let-7b expression was found in BC patients with high DRC versus the remaining groups p < 0.001. Thus, our data reveal a possible role of Let-7b on DRC during breast carcinogenesis. Our study is innovative because it provides the first evidence that Let-7b may play role in DRC regulation through the NER repair pathway in BC. View Full-Text

Keywords: breast cancer; DNA repair; nucleotide excision repair pathway; Let-7b breast cancer; DNA repair; nucleotide excision repair pathway; Let-7b





Autor: Jarline Encarnación 1, Carmen Ortiz 1, Ralphdy Vergne 2, Wanda Vargas 1, Domenico Coppola 3 and Jaime L. Matta 1,*

Fuente: http://mdpi.com/



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