https://www.selleckchem.com/products/sc-43.html Upregulation of miR-199b-5p and miR-101-3p inhibited the viability and promoted the apoptosis in TSCCA and SCC-9 cells, as shown by the CCK8 assay and flow cytometry analysis, respectively. Inhibition of BICC1 reduced viability and promoted apoptosis in TSCCA cells. Additionally, the relationship between BICC1 and both miR-101-3p and miR-199b-5p was assessed by a luciferase reporter assay. The effects of miR-101-3p and miR-199b-5p upregulation on the promotion of cell apoptosis and the inhibition of tumor growth were reversed by overexpression of BICC1. In conclusion, the increased levels of miR-199b-5p and miR-101-3p enhanced apoptosis and suppressed cell viability in oral cancer by suppressing BICC1 expression. Over the last year, in response to public outcry, the US Congress has taken a special interest in-and held several hearings on-prescription drug prices. While this is a welcome move, these debates largely ignore prudent discussions surrounding exorbitant health expenses associated with approved novel cancer drugs. In this commentary, we argue that significant financial burden associated with these promising therapies is a reminder of how increasing utilization of these medications-without regard to unbiased distribution-specifically breeds unintended consequences, such as racial and ethnic health inequities. Additionally, we elucidate how variations in access to novel cancer treatments may even exacerbate current health inequities. Our editorial also highlights how inequitable dissemination of novel cancer drugs takes place along racial and socio-economic lines and how this leads to financial toxicities and other adverse consequences. We introduce a novel and an innovative research framework for investigators that can be used in research projects that aim to understand the dissemination of novel therapies. Nowadays we can find a number of experiments that have showed the importance of learning in several situa