Expression signature of lncRNA APTR in clinicopathology of breast cancer: Its potential oncogenic function in dysregulation of ErbB signaling pathway

A growing amount of evidence has revealed that long noncoding RNAs (lncRNAs) play significant roles in malignancies through different mechanisms especially the competing endogenous RNA (ceRNA). They have also been shown to have the potential diagnostic, prognostic and therapeutic biomarker capacity in oncology research. Recently, lncRNA Alu-mediated p21 transcriptional regulator (APTR) has been proposed as an oncogenic lncRNA in development and clinical outcome of some cancers. However, clinical and molecular importance in breast cancer (BC) is still unclear. The purpose of this study was to examine the APTR expression and its potential roles in BC. The 47 BC tumors and 47 tumor adjacent normal tissues were obtained from the study subjects. Real-time PCR was applied for the analysis of APTR expression in breast tumors compared with paired adjacent normal tissues. Then, we used bioinformatics approach to investigate the potential ceRNA activity of APTR in APTR-microRNAs-mRNAs axes and with focus on ErbB signaling pathway in BC. Our results demonstrated that APTR expression was significantly upregulated in BC tumors compared with the adjacent normal tissues. Besides, APTR over-expression was related to a larger tumors size. Finally, bioinformatics analysis indicated that APTR could influence cell proliferation through dysregulating the oncogenes working in ErbB signaling pathway by sponging some tumor suppressive microRNAs (miRNAs). Current work provided some clues for the involvement of APTR in physiopathology of the breast tumors. However, other aspects of these findings need to be further elucidated by future functional studies. •LncRNA APTR expression is profoundly upregulated in breast tumors compared with the adjacent normal tissues.•APTR upregulation is significantly related to a larger size of the BC tumors.•Bioinformatics analysis indicated that APTR could influence cell proliferation through sponging some tumor suppressive microRNAs