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News in brief

New research from the Carnegie Institution (MD, USA) and collaborators demonstrates that a small miRNA cluster, known as miR-17~92, could play a key role in retinoblastoma development. Their work, published in Genes & Development, suggests that miR-17~92 could be a potential therapeutic target for treating this rare form of childhood cancer, and possibly other cancers too. Previous research has shown that, in other forms of cancer such as lymphoma and leukemia, aberrant versions of miR17~92 are involved in preventing precancerous cells from undergoing apoptosis and reducing the levels of a tumor-suppressing protein called PTEN. This new study suggests that the oncogenicity of miR-17~92 is context specific, owing to the team’s discovery that, in retinoblastoma, miR17~92 synergizes with loss of Rb tumorsuppressor gene family members in order promote tumor development. The team observed miR-17~92 genomic amplifications in all human retinoblastomas examined, in addition to in some mice in murine retinoblastoma models. The group engineered mice to express high levels of miR-17~92 in their retinas. While miR-17~92 was found to be dispensable for retinal development, miR-17~92 overexpression in Rb/p107-deficient retinal cells led to rapid progression of retinoblastoma, with frequent metastasis to the brain. In this study, deletion of Rb family members was found to lead to compensatory upregulation of the cyclin-dependent kinase inhibitor p21Cip1, which is able to compensate for the loss of Rb protein function. miR-17~92 overexpression was found to counteract p21Cip1 upregulation, consequently promoting proliferation and driving retinoblastoma formation. “These findings – which show that miR-17~92 overcomes the cell’s attempts to compensate for the loss of Rb – could be similar in other types of cancers,” explains David MacPherson, an author of the study. “This microRNA cluster could represent a new therapeutic target for treating tumors caused by Rb deficiency.”