Tzitzijanik Madrigal Domínguez completed her Graduation in Biology from Universidad Autonoma Metropolitana (UAM) in 2010; studied at Molecular Oncology Laboratory and received her MA in Experimental Biology from UAM in 2013. She is currently a PhD student in Experimental Biology Program-UAM. She is a Member of Mexican Association for Cancer Research which is a civil association, made up of scientists recognized both nationally and internationally as leaders in the development of basic, clinical, pharmacological and social research projects associated with the study of cancer.
p53 is a tumor suppressor protein encoded by the TP53 gene which is located in chromosome 17p13.1. In response to environmental and cellular stress p53 activates the expression of genes and microRNAs (miRNAs) involved in cell cycle arrest, senescence and apoptosis. Th e TP53 is the most frequently mutated gene in human cancers. It has also been demonstrated that some mutant p53 proteins not only lose tumor suppressor activity, but also acquire novel oncogenic functions also known as “gain of function” (GOF) that are independent of wild-type (WT) p53. Recent studies have shown that mutant p53 can regulate gene expression and exert oncogenic eff ects through specifi c miRNAs. We transfected p53 mutants (p53R273, p53R175H, p53R248Q) into p53-null Saos2 cells, profi led the miRNA expression by miRNA PCR array, we selected and validated the expression of miR-182, miR-200b, miR- 3151 and miR-509-5p by real-time quantitative PCR and observed that mutants of p53 have a global negative eff ect for human miRNome expression, however some miRNAs were upregulated. Here we found tumor suppressors miRNAs downregulated like miR-200b, miR- 3151 and miR-509-5p or oncomiRNAs like miR-182 upregulated. Many studies have reported that patients with tumors carrying p53 mutations have worse prognosis and poorer response to conventional anticancer treatments that those bearing p53 WT protein, therefore, our study contributes to the understanding of regulation of miRNAs by mutants of p53 that could explain in part the role of mutant p53 proteins in the development of cancer and may help propose new target therapies.
Wenbin Li completed his PhD in Plant Genetics and Breeding in 1988 at Northeast Agricultural University of China. He is working at Soybean Research Institute of Northeast Agricultural University for more than 15 years as a Director and Professor. His major research areas are covered by soybean functional genomics, gene characteristics for agronomic important traits, and molecular breeding. He has published over 80 peer reviewed papers in numbers of international journals, such as New Phytologist, The Plant Journal, TAG, BMC Genomics and Heredity. Recently, he became a member of Executive Committee for World Soybean Association, and an Associate Editor of BMC Genomic.
Disease resistance and seed quality are important traits for soybean breeding. Better understanding of the genetic architecture and genomic landscape of soybean germplasm with targeted traits is the precondition of molecular design breeding of soybean. Construction of a favorable data platform including phenotyping and genotyping pools and effi cient analytical approaches were the fundamental tasks for molecular breeding work. Th erefore, more than 500 diverse soybean accessions were sequenced using specifi c-locus amplifi ed fragment sequencing (SLAF-seq) to establish a genotype database. In total, 64 141 single nucleotide polymorphisms (SNPs) with minor allele frequencies (MAFs) > 0.05 were found among the 512 tested accessions. Th e genotyped soybean germplasm has been phenotyped for some important soybean quality traits including soybean fatty acid components and seed vitamin E content under multi-environmental conditions. Resistance to diff erent pathogens including resistance to soybean cyst nematode (SCN), soybean white mold (SWM), soybean root rot (SRR) and soybean mosaic virus (SMV) has also been phenotyped. A set of loci were found to be associated with the above traits by GWAS and some of them were confi rmed by bi-parental mapping which has been used for molecular assisted selection breeding. A set of candidate genes for disease resistance that have been evaluated via sequence polymorphism and diff erential expression in special donors were cloned and were staged in functional genomics research.