We suggest miR-223 may promote colon cancer cell invasion and metastasis by downregulating p120, thereby reducing intercellular adhesion, promoting RhoA activity, and activating β-catenin signaling.
<b>Methods:</b> Expression of plasma miR-21, miR-23b, miR-27a, miR-143, miR-146a, and miR-223 was measured in 48 persons with seropositive and/or erosive RA (mean DAS-28-ESR 3.0, SD 1.4) and 23 age-, sex-, and BMI-matched healthy controls.
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.
Colon cancer is one of the most common malignancies worldwide, while the molecular mechanism remains largely unknown. miR-223-3p plays an important role in cancer development.
In this explorative study, we describe miRNA-based models, which included miRNA expression values together with PSA levels, that increased the classification function of the PSA screening test with diagnostic and/or prognostic potential: [PSA + miR-142-3p + miR-142-5p + miR-223-3p] model (AUC:0,821) to discriminate PCa from BPH (Sn:91,7% Sp:42,9% vs Sn:100% Sp:14,3%); and [PSA + miR-342-3p + miR-374b-5p] model (AUC: 0,891) to discriminate between GS ≥ 7 tumours and men presenting PSA ≥ 4 ng/ml with no cancer or GS6 tumours (Sn:81,8% Sp:95% vs Sn:54,5% Sp:90%).
Taken together, miR-223 can regulate tumorigenesis at multiple levels, including by suppressing the inflammatory tumor microenvironment and modulating malignancy of cancer cells.
MiR-223-3p is involved in the regulation of a broad range of cellular processes and in many types of pathological processes as cancer, autoimmune and inflammatory diseases.
We also discovered that cancer cells deficient in BRCA1 or its obligate partner BRCA1-Associated Protein-1 (BAP1) routinely repress miR223-3p to permit repair of stressed replication forks via aNHEJ.
Using ddPCR technology, miR-223 was externally validated as a reproducible, effective serum biomarker of early-stage NSCLC in ethnically different subjects.
In renal cancer cells, overexpression of miR-223-3p enhanced cell proliferation and metastasis, while inhibition of miR-223-3p reduced the malignant capacity of the cells.