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.
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.
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.
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.
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.
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.
The analysis of miR-223 predicted targets revealed enrichment in cell death and survival-related genes and in pathways frequently altered in breast cancer.