The analysis of miR-223 predicted targets revealed enrichment in cell death and survival-related genes and in pathways frequently altered in breast cancer.
The expression of miR-21, miR-29a, miR-142-3p and miR-223 increased in myeloid cells during tumor progression in mouse models of breast cancer and melanoma metastasis.
Accordingly, both RT-induced miR-223 and peri-operative inhibition of EGFR efficiently prevented BC cell growth and reduced recurrence formation in mouse models of BC.
In previous study, we found that miRNA-223 was significant expression inexosome derived from peripheral blood serum of breast cancer patients than in samples from control subjects, Therefor,the role ofmiRNA-223willbe researched in MCF-7 breast cancer cells.In this study, to explore the role of miRNA-223in influencing cell proliferation, metastasis and invasion of breast cancer, TargetScan tools (http://www.targetscan.org/vert_71/) was used to scan target genes of miRNA-223, and thenmiRNA expression, real time PCR, Western blotting andluciferase report assay were used to test regulates relationship of miRNA-223and its targets,cell viability and BrdU analysiswere used to test cell proliferation of MCF-7 breast cancer cells after expression miRNA-223inhibitor.
Collectively these findings suggested that the inactivation of the NLRP3 inflammasome driven by miR‑223‑3p reduced the growth and immunosuppression of breast cancer in vitro and in vivo, and may represent a novel therapeutic strategy in treating breast cancer.
We show that STIM1 expression is regulated post-transcriptionally by the miRNA machinery and identify miR-223 and miR-150 as regulators of STIM1 expression in the luminal non-aggressive MCF7 breast cancer cell line.
MiR-223-3p targets and inhibits the expression of ECT2, thus inhibiting the invasion and migration of BC cells, and promoting cell apoptosis. miR-223-3p plays a protective role in BC.