Altered expression of long noncoding RNAs and p53 as a possible genetic signature in luminal A invasive breast ductal carcinoma

Breast cancer is the second most common cause of cancer-related death among females. The long non-coding RNAs (lncRNAs) are a significant population of non-coding RNAs with well-defined functions in both adjacent normal cells and tumorigenesis. Miss expression of them has been associated with the development of different kinds of cancers.

The aim of this study was to investigate the alterations in 3 lncRNAs and p53 in tissue samples of a group of women with luminal type A breast adenocarcinoma.

In this case-control study, the expression levels of p53 and three lncRNAs were evaluated in association with luminal A breast cancer in 80 ductal carcinoma tumors and adjacent normal breast tissues.Quantitative real-time PCR was used to measure the expression of the mentioned genes. The data were analyzed using t-tests.

The expression levels of IGFBP7-AS1, and RHPN1-AS1, showed a significant increase (P>0.05) while P53 and LINC00861 had a significant decrease in expression level in tumor tissues compared to adjacent normal tissues (P> 0.05). Receiver Operating Characteristic (ROC) curve indicated the diagnostic power of LINC00861 in differentiating tumor tissues from adjacent normal tissue with 90% sensitivity and 96% specificity, which can also interact with P53.Based on the area under the curve (AUC) value, expression of Linc00861, p53, RHPN1-AS1, and IGFBP-AS1 genes can help to differentiate patients from healthy individuals with diagnostic power of 0/855, 0/824, 0/778, and 0/659, respectively.

The key roles of the latest genes in the control of cancer-related pathways and the dysregulation of their expression in studied malignancies imply that they can be exploited as biomarkers for cancer diagnosis, prognosis, and possible therapeutic targets. Here, the roles of lncRNAs in invasive breast ductal carcinoma type luminal A and their importance in prognosis and patient treatment are discussed.