Stefan Costinean

TL;DR: The enforced expression of miR-29s in lung cancer cell lines restores normal patterns of DNA methylation, induces reexpression of methylation-silenced tumor suppressor genes, and inhibits tumorigenicity in vitro and in vivo.

TL;DR: The data suggest that the LPS/TNF-α-dependent regulation of miR-155 and miR -125b may be implicated in the response to endotoxin shock, thus offering new targets for drug design.

TL;DR: It is reported that miR-221&222 are overexpressed in aggressive non-small cell lung cancer and hepatocarcinoma cells, as compared with less invasive and/or normal lung and liver cells, and it is demonstrated that the MET oncogene is involved in miR+222 activation through the c-Jun transcription factor.

TL;DR: It is demonstrated that deletion of mouse Mir122 resulted in hepatosteatosis, hepatitis, and the development of tumors resembling HCC, demonstrating critical functions for miR-122 in the maintenance of liver homeostasis and have important therapeutic implications, including the potential utility of mi R-122 delivery for selected patients with HCC and the need for careful monitoring of patients receiving miR -122 inhibition therapy for HCV.

TL;DR: Data show that methylation-dependent tissue-specific regulation of the lncRNA MEG3 by miR-29a may contribute to HCC growth and highlight the inter-relationship between two classes of non-coding RNA, miRNAs and lncRNAs, and epigenetic regulation of gene expression.