The participation of miR-137 in tumorigenesis is not restricted to glioblastoma. Similar to what has been observed in glioblastoma cells, restoration of miR-137 reduced cell proliferation of colon cancer lines HCT116 and RKO. Regulation of miR-137 expression via promoter hypermethylation is perhaps a common mechanism as it was also established in oral cancer, gastric cancer and squamous cell carcinoma of head and neck. Uveal melanoma is another tumor type affected by miR-137 where its expression is lower in uveal melanoma cell lines when compared to uveal melanocytes. Ectopic expression of miR-137 in melanoma cells induced G1 cell cycle arrest and a decrease in cell growth. A connection between miR-137 and breast cancer has been suggested based on its regulation of orphan nuclear receptor ERRa, a prognostic factor of poor clinical outcome. Downregulation of ERRa mediated by miR-137 impaired proliferative and migratory capacity of breast cancer cells. In addition, ectopic expression of miR-137 in lung cancer cells induced G1 cell cycle arrest and decreased cell growth in vivo and in vitro. Clearly, miR-137 is an important player in a diverse set of cancer systems and further understanding of its mechanism of action and its mRNA targets are warranted. Several miR-137 targets have been identified in the context of the neuronal system including lysine-specific demethylase, BKM120 RTVP-1, KDM1A, Mind Bomb-1, COX-2, the histone methyltransferase Ezh2, the cell cycle regulator CDK6, the oncogenic RNA binding protein Musashi1, CSE1 chromosome segregation 1-like and Jarid1b, a histone H3 Lys4 demethylase. However, determining the genome-wide impact miR-137 transfection would have on glioblastoma cells is a mandatory step to establish its potential as a therapeutic agent. We have conducted genomic analyses in glioblastoma cells including the usage of a novel approach inspired by the recently described mechanism of miRNA action via PABP and the poly A tail. Our results led to the identification of 595 targets of miR-137, comprising important oncogenic proteins such as cKIT, AKT2, YBX1, CD24, CDC42 and TGFb2. We also determined that miR-137 potentially shares a large portion of its targets with miR-7, miR-124 and miR-128, indicating that their absence as a group in neuronal cells could constitute an important contribution to gliomagenesis. Several approaches are available to identify miRNA targets, starting with multiple target prediction methods and continuing with a variety of biological procedures that include reporter based screenings, BMN673 shotgun proteomics, transcriptomic analyses and Ago2 based immunoprecipitation methods. Although in silico predictions are becoming more accurate, they will never substitute biological methods. No single approach is comprehensive enough; the advantages of employing dual approaches can be illustrated by the miR-122 target analysis that we conducted using luciferasebased screening in combination with APEX shotgun proteomics. In the current study, we also used a dual strategy to evaluate the impact of miR-137 in glioblastoma cells. The novelty was the usage of PABP as a reporter of miRNA activity.