To investigate the expression of miR-21, miR-221, miR-143, and miR-106a in patients' osteosarcoma samples, and to explore the correlation between these microRNAs (miRNAs) and the clinical stage of osteosarcoma.
To our knowledge, it was the first time to target Bcl-2 directly to explore the underlying mechanism by which miR-143 performed its role to induce apoptosis in tumor cells, thus improving osteosarcoma progression.
The delivery efficiency of exosome-formed miR-143 was less than that achieved with lipofection, but the migratory potential of osteosarcoma cells was similarly inhibited after both strategies.
Our results suggest that TGF-β1 up-regulates versican expression by suppressing miR-143, and this pathway is important for osteosarcoma cell migration and invasion.
Taken together, our data suggest that miR-143 inhibits EGFR signaling through its downstream ERK/MAPK signaling cascades to control MMP9 expression in OS.
The results showed that circulating levels of miR-21 were significantly higher in osteosarcoma patients than controls, while miR-199a-3p and miR-143 were decreased in osteosarcoma patients.
These effects were associated with decreased expression of Notch-1 and its downstream genes, such as vascular endothelial growth factor and matrix metalloproteinases, as well as increased expression of a panel of tumor-suppressive microRNAs (miRNAs), including miR-34a, miR-143, miR-145 and miR-200b/c that are typically lost in osteosarcoma.
Taken together, these data indicated that the downregulation of miR-143 correlates with the lung metastasis of human osteosarcoma cells by promoting cellular invasion, probably via MMP-13 upregulation, suggesting that miRNA could be used to develop new molecular targets for osteosarcoma metastasis.