C-Myc negatively controls the tumor suppressor PTEN by upregulating miR-26a in glioblastoma multiforme cells

Abstract

The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with oncogenesis in GBM through deregulation of miRNAs via the c-Myc-miR-26a-PTEN signaling pathway. This may be of clinical relevance.

Keywords: 3′-UTR; 3′-untranslated region; AML; B-cell lymphoma; BCL; C-Myc; CCK-8; Cell Counting Kit-8; GBM; Glioblastoma multiforme; MiR-26a; PTEN; Proliferation; acute myeloid leukemia; glioblastoma multiforme; miRNA; microRNA; phosphatase and tensin homolog located on chromosome 10.