OncogenesResearch has shown that mi

OncogenesResearch has shown that miRNAs can function as oncogenes, promoting abnormal cell growth and contributing to tumor for- mation. These miRNAs may directly inhibit the activity of tumor suppressors or work indirectly by removing the genetic brakes on oncogene activity. For example, miR-155 can promote abnormal B cell proliferation, setting in process a series of changes that eventually lead to the development of leukemia and lymphoma (Babar et al., 2012; O’Connell et al., 2009). Impor- tantly, delivery of antimiRs targeting miR-155 can inhibit tumor growth (Babar et al., 2012; Cheng et al., 2015) (Figure 1A). Another miRNA, miR-21, is overexpressed in pre B cell lym- phoma and has been implicated in other cancers, such as lung cancer, through targeting negative regulators of Ras signaling (Hatley et al., 2010; Medina et al., 2010). In glioblastomas, an oncogenic miRNA, miR-10b, is expressed at higher levels than in normal brain tissue and is required for tumor growth (El Fatimyt al., 2017). These oncogenic miRNAs exhibit the phenomenon of oncogene addiction (oncomiR addiction), because the tumors are dependent on the continued expression of the miRNAs for survival (Cheng and Slack, 2012), and are, thus, important poten- tial targets in anti-cancer therapy. Recently, the potential for targeting oncomiRs uniquely overexpressed in an individual pa- tient’s tumors was demonstrated, opening the way to personal- ized miRNA therapy as we discuss at the end of the review (Gilles et al., 2018).