In particular, the most differentially expressed miRNAs were validated by qRT-PCR, such that miR-200a-3p and miR-96-5p were up-regulated and miR-1-3p and miR-486-3p were down-regulated in patients with breast cancer with SLN metastasis.
We previously demonstrated that miR-96 has a suppressive effect on breast cancer aggressiveness and that this effect was mediated by ABCE1 gene regulation.
Also, it is important to indicate that some exosomal miRNAs including miR-126, miR-122, miR-92-1, miR-19a, and miR-29c together with circular miRNAs, such as miR-21-5p, miR-96-5p, and miR-125b-5p can provide a promising evaluation route in breast cancer prognosis.
miR-96 is reported to inhibit reversion cysteine-rich Kazal motif (RECK), which is associated with tumor invasion, in solid cancer types (e.g. breast cancer, non-small cell lung cancer, esophageal cancer).
Respectively, three, three, three, and seven genes were found to have binding sites for miR-7, miR-9, miR-96, and miR-182 and were associated with breast cancer.
However, other functions of miR-96-5p in breast cancer, particularly those that are associated with autophagy, remain unknown. miR-96-5p expression was demonstrated to be upregulated in breast cancer cells compared with in normal breast epithelial cells.
Furthermore, we explored the molecular mechanisms by which miR-96 contributes to breast cancer progression and identified PTPN9 (protein tyrosine phosphatase, non-receptor type 9) as a direct target gene of miR-96.
Ten miRNAs were selected for further investigation, of which 4 (miR-505-5p, miR-125b-5p, miR-21-5p, and miR-96-5p) were significantly overexpressed in pretreated patients with breast cancer compared with healthy individuals in 2 different series of plasma.
We found that expression of miR-96 was commonly upregulated in breast cancer cells and breast cancer specimens when compared with that in non-malignant breast epithelial cells and adjacent normal tissues.