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Candiolo, Italy

Pierantoni G.M.,University of Naples Federico II | Conte A.,University of Naples Federico II | Rinaldo C.,University of Rome La Sapienza | Tornincasa M.,University of Naples Federico II | And 5 more authors.
Oncotarget | Year: 2015

The mitotic spindle assembly checkpoint (SAC) is an essential control system of the cell cycle that contributes to mantain the genomic stability of eukaryotic cells. SAC genes expression is often deregulated in cancer cells, leading to checkpoint impairment and chromosome instability. The mechanisms responsible for the transcriptional regulation and deregulation of these genes are still largely unknown. Herein we identify the nonhistone architectural nuclear proteins High Mobility Group A1 (HMGA1), whose overexpression is a feature of several human malignancies and has a key role in cancer progression, as transcriptional regulators of SAC genes expression. In particular, we show that HMGA1 proteins are able to increase the expression of the SAC genes Ttk, Mad2l1, Bub1 and Bub1b, binding to their promoter regions. Consistently, HMGA1-depletion induces SAC genes downregulation associated to several mitotic defects. In particular, we observed a high number of unaligned chromosomes in metaphase, a reduction of prometaphase time, a delay of anaphase, a higher cytokinesis time and a higher percentage of cytokinesis failure by using live-cell microscopy. Finally, a significant direct correlation between HMGA1 and SAC genes expression was detected in human colon carcinomas indicating a novel mechanism by which HMGA1 contributes to cancer progression. Source


Castellanos T.,Laboratorio Of Nutrigenomica | Rodriguez D.,Laboratorio Of Oncogenomica
Revista Chilena de Nutricion | Year: 2015

For some years a boom in the field of nutrition related to the beneficial effect of consuming omega-3 fatty acids to human health has taken place. Currently, we can fi nd a variety of supplements in capsules with omega 3 with or without vitamins, minerals and other substances, as well as several foods fortifi ed with omega 3. Many of the scientific research shows that eating certain doses of these fatty acids may have a benefi cial effect on diseases like lupus erythematosus, diabetes mellitus type 2, cancer, atherosclerosis, hyperlipidemia, metabolic syndrome, and others. Due to the strength of its benefi cial effect on cardiovascular disease different international associations issued recommendations for consumption. However, these recommendations, there are some considerations arising from current studies by eating them. So this review aims to give an update on the issue and make account possible disputes arising from the use thereof. © 2015, Sociedad Chilena de Nutricion Bromatologia y Toxilogica. All rights reserved. Source


Peralta R.,Laboratorio Of Oncogenomica | Valdivia A.,Laboratorio Of Oncogenomica | Alvarado-Cabrero I.,Hospital de Oncologia | Gallegos F.,Servicio de Cabeza y Cuello | And 8 more authors.
Journal of Clinical Pathology | Year: 2012

Aims: The authors have previously reported that cellular retinol-binding protein 1 (CRBP1) gene gain and its expression correlated significantly with survival in laryngeal carcinoma patients. The authors hypothesised that inactivation of the CRBP1 gene through CpG methylation is associated with patient status and gene expression. In this work, the authors determine the expression and methylation status of the CRBP1 gene and its correlation with clinical variables of laryngeal carcinoma patients. Methods: The CRBP1 gene methylation promoter was assessed by methylation specific PCR analysis in tissue samples from larynx cancer specimens and its expression was assessed by immunohistochemistry on paraffin embedded tissue using tissue microarray. The results were then compared with the clinical pathological variables and outcome measures. The study included 46 samples from patients with non-metastatic squamous cell carcinoma of the larynx without any previous oncological treatments. Results: Lack of CRBP1 expression was seen in 17 of the 46 laryngeal carcinoma samples, while the remaining 29 samples showed increased expression. Significant associations were found between CRBP1 expression and methylation and patient status. There was a tendency for association in all clinical stages of the disease. CRBP1 gene expression and its unmethylated promoter correlated significantly with survival (p<0.05). Conclusions: An early event of larynx cancer could be CRBP1 expression related to unmethylation of the promoter region. These features could also be associated with good response and survival. The authors hypothesised that increased expression and unmethylated promoter of the CRBP1 gene could be considered as markers for larynx cancer. Source


Mendoza-Rodriguez M.,Laboratorio Of Oncogenomica | Mendoza-Rodriguez M.,Research Center Estudios Avanzados | Mendoza-Rodriguez M.,National Polytechnic Institute of Mexico | Arreola H.,Laboratorio Of Oncogenomica | And 11 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2013

Aims: Cervical Cancer (CC) is one of the most important health problems in women. It frequently presents genetic changes at chromosome region 3q21. This region contains the Cellular Retinol Binding Protein 1 gene (CRBP1) which has been implicated as an important element in the development of other types of cancer. The main goal of the present work was to determine the molecular alterations of CRBP1 and its relationship to CC. Methods: To determine the molecular alterations of CRBP1 gene in CC; twenty-six CC and twenty-six healthy cervix samples were evaluated for: 1) Copy number gain by real-time PCR analysis, 2) expression levels by an immunohistochemistry assay on tissue microarray, and 3) the methylation status of the CRBP1 promoter region. Results: The increase in CRBP1 copy number was observed in 10 out of the 26 CC samples analyzed, while healthy cervices samples showed no changes in the copy number. In addition, there was a lack of expression of the CRBP1 gene in an important number of the CC samples (17/26), and the CRBP1 gene promoter was methylated in 15/26 of the CC samples. Interestingly, there was a significant association between the lack of expression of the CRBP1 gene and its methylation status. Conclusions: The data indicates that, both activating and inactivating changes in the CRBP1 gene could be significant events in the development and progression of CC, and the lack of expression of the CRBP1 protein could be related with to the development of CC. We believe that there is enough evidence to consider to CRBP1 gene as a tumor suppressor gene for CC. Source


Marrero D.,Laboratorio Of Oncogenomica | Marrero D.,Autonomous University of Ciudad Juarez | Peralta R.,Laboratorio Of Oncogenomica | Valdivia A.,Laboratorio Of Oncogenomica | And 14 more authors.
Journal of Clinical Pathology | Year: 2012

Aims: Neurofibromin 1 (NF1) as a tumour suppressor gene can give rise to several transcripts by an alternative splicing event, generated at least for CELF cofactors. At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect NF1 gene expression, the NF1 isoform ratio and the CELF transcripts present in sporadic breast cancer. Methods: Neurofibromin and RAS expression were analysed on tissue microarrays containing sporadic breast cancer (n=22), benign lesions (n=18, including six fibroadenomas, six fibrocystic changes and six ductal hyperplasias) and normal breast tissue (n=6) by immunohistochemistry assay. NF1 and CELF 3-6 RNA expression was performed by end point reverse transcription-PCR in the breast samples. Results: NF1 and RAS expression in breast tissues showed no differential expression by immunohistochemistry results. Interestingly, the authors observed a shift transition in the isoform transcripts, from type II in normal breast tissue to type I isoform in breast carcinomas. CELF cofactor expression failed to be related with the shift transition of NF1 in breast tissues. Conclusions: These data suggest that there is a tendency for an NF1 expression shift transition from type II to type I isoform, which could comprise a significant event in the development and progression of sporadic breast cancer. This shift transition may not be related with CELF cofactors. Source

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