Expression of Treg-associated lncRNAs in breast cancer

Regulatory T cells (Tregs) have important functions in tumor microenvironment, particularly for induction of immune evasion. In order to find the underlying mechanism of dysregulation of Tregs in breast cancer tissues, we designed the current study to appraise expression of five Treg-related long non-coding RNAs (lncRNAs), namely FLICR (FOXP3 Regulating Long Intergenic Non-Coding RNA), NEST (IFNG-AS1), RMRP (RNA Component of Mitochondrial RNA Processing Endoribonuclease), MAFTRR (MAF Transcriptional Regulator RNA) and TH2-LCR (Th2 Cytokine Locus Control Region) in paired breast cancer and nearby noncancerous tissues. Expression levels of RMRP, TH2-LCR, MAFTRR and GATA3-AS1 were significantly higher in breast cancer samples compared with non-tumoral tissues. The calculated AUC values for GATA3-AS1, TH2-LCR, RMRP and MAFTRR were 0.66, 0.63, 0.63 and 0.60, respectively. There were significant positive associations between expression level of RMRP gene in tumor tissues and nuclear grade, tubule formation and tumor sizes. In addition, there was a significant positive association between expression levels of MAFTRR genes in tumor tissues and nuclear grade. Besides, expression levels of FLICR were different among tumors with different levels of HER2/neu receptor. Taken together, Treg-associated lncRNAs might contribute to the pathogenesis of breast cancer.

Automated summary

This study evaluated the expression of five Treg-related long non-coding RNAs in breast cancer tissues. The results showed significantly higher expression levels of RMRP, TH2-LCR, MAFTRR, and GATA3-AS1 in breast cancer samples compared to non-tumoral tissues. Positive associations were found between the expression levels of RMRP and MAFTRR genes in tumor tissues and certain tumor characteristics. Additionally, differences in FLICR expression were observed among tumors with different levels of the HER2/neu receptor. These findings suggest that Treg-associated lncRNAs may contribute to the pathogenesis of breast cancer.