Abstract
Glioblastoma multiforme (GBM) is the most common and lethal cancer of the adult brain, remaining incurable with a median survival time of only 15 months. In an effort to identify new targets for GBM diagnostics and therapeutics, recent studies have focused on molecular phenotyping of GBM subtypes. This has resulted in mounting interest in microRNAs (miRNAs) due to their regulatory capacities in both normal development and in pathological conditions such as cancer. miRNAs have a wide range of targets, allowing them to modulate many pathways critical to cancer progression, including proliferation, cell death, metastasis, angiogenesis, and drug resistance. This review explores our current understanding of miRNAs that are differentially modulated and pathologically involved in GBM as well as the current state of miRNA‐based therapeutics. As the role of miRNAs in GBM becomes more well understood and novel delivery methods are developed and optimized, miRNA‐based therapies could provide a critical step forward in cancer treatment.
Highlights
Glioblastoma multiforme (GBM) is the most common and lethal cancer of the brain, with approximately 10,000 newly diagnosed cases each year in the United States [1]
Restoration of miR-152 is able to reduce proliferation, migration, and invasion, as well as induce apoptosis of GBM cancer stem cells (GSCs). These activities are mediated through targeting of Krüppel-like factor 4 (KLF4), which is associated with downregulation of LGALS3 and reduced activation of the MEK1/2 and PI3K signaling pathways
The understanding of miRNAs is rapidly developing with potential to drastically change the conceptualization of developmental biology, including the development of pathological conditions such as cancer
Summary
Glioblastoma multiforme (GBM) is the most common and lethal cancer of the brain, with approximately 10,000 newly diagnosed cases each year in the United States [1]. In GBM, miR-7 is frequently downregulated, allowing for enhanced activation of the Akt pathway, and increased viability and invasiveness of tumor cells [23, 24]. Restoration of miR- 34a can reduce CDK6 protein expression, inhibiting cell survival, proliferation, and invasion as well as inducing apoptosis [31, 32].
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