The association between miR-204-5p expression and clinical outcomes of patients with breast cancer showed a nonlinear pattern that was reproduced in experimental assays of cancer cell behavior and metastatic capacities.
The expression of miR-204 was decreased, while AREG and p-AKT was increased in T3 stimulated BC cell lines.T3 stimulation promoted cell viability. miR-204 targets AREG to regulate its expression.
The outcome of the SMD from meta‑analysis also indicated that the expression of miR‑204‑5p was markedly reduced in 2,306 BC tissue samples in comparison to 367 para‑carcinoma tissue samples.
Higher H19 (P = 0.001) along with lower miR-675 (P = 0.007) levels and higher miR-204 (P = 0.017) along with lower NEAT1 (P = 0.030) levels were detected in plasma of HER2-positive patients compared with the other BC subgroups.
Kaplan‑Meier survival analysis revealed that six DElncRNAs (INC AC112721.1, LINC00536, MIR7‑3HG, ADAMTS9‑AS1, AL356479.1 and LINC00466), nine DEmRNAs (KPNA2, RACGAP1, SHCBP1, ZNF367, NTRK2, ORS1, PTGS2, RASGRP1 and SFRP1) and two DEmiRNAs (hsa‑miR‑301b and hsa‑miR‑204) had significant effects on overall survival in BC.
In conclusion, the present study suggested that ATXN8OS acts as a tumour promoter by sequestering miR‑204 during the development of BC, therefore providing a mechanistic insight which may facilitate the diagnosis and treatment of BC.
Subsequently, we demonstrated that ARNILA functioned as a competing endogenous RNA (ceRNA) for miR-204 to facilitate expression of its target gene Sox4, which is known to induce EMT and contribute to breast cancer progression, thereby promoting EMT, invasion and metastasis of TNBC.
In the present study, we integrated the results of microarray analyses of breast cancer tissues obtained from an online database with our own determination of the expression of miR-204 in breast cancer MCF-7 cells using real-time qPCR (RT-qPCR).
In conclusion, the frequent upregulation of Six1 and/or downregulation of miR-204-5p in breast cancer may shift the equilibrium of these reciprocal regulations and lock breast cancer cells in the mesenchymal state.
In conclusions, miR-204 targets JAK2 and suppressed JAK2 and p-JAK2 expression in breast cancer, which further inhibit the activation of STAT3, BCl-2 and survivin.