چکیده
|
Introduction: Breast cancer is the most common malignancy in women worldwide and the second most common cancer after
lung cancer. Breast cancer is a multifactorial disease resulting from the interaction of genetic and environmental factors.
About 10% of breast cancers are hereditary and inherited mutations with high sensitivity and high penetrating are seen in
genes such as BRCA1, BRCA2 and TP53. P53 gene is a transcription factor phosphoprotein that regulates the expression
of more than 2322 target genes. It is involved in different cellular processes such as maintaining genome stability, longevity,
metabolism and above all tumor suppressor. P53 mutations are found in almost half of all human tumors , and it seems that
the rest of the tumors also may be due to defects in pathways associated with P53. Recently, the role of a natural antisense
P53 has been known as WRAP53, which has an important role in post-transcriptional regulation. WRAP53 mRNA also
functions as a p53 antisense transcript that regulates endogenous p53 mRNA levels and further induction of p53 protein by
targeting the 5’ untranslated region of p53 mRNA. This gene encodes both (WRAP53α) which is an antisense transcript
and stabilizes the tumor suppressor p53 and a protein (WRAP53β) which helps the maintenance of Cajal bodies, DNA
repair and telomere elongation. WRAP53β, which is the concern of the present study, is one of the many proteins containingWD40
domains. These proteins do not have enzymatic activity, but they act as platforms for the collection of large complexes
of proteins and RNAs, so facilitate the interactions between Cajal body factors and DNA repair proteins. This gene is
located on chromosome 17 in a head to head with P53 geneWRAP53 has 3 start exons. Inspired by the previous studies, the
researcher intended to evaluate the WRAP53β splice variant in breast tumoral tissue samples of breast cancer patients.
Materials and methods: In this study 30 fresh tumoral and marginal tissues of b
|