Abstract
Glioblastoma multiforme (GBM), an aggressive tumor that typically exhibits treatment failure with high mortality rates, is associated with the presence of cancer stem cells (CSCs) within the tumor. CSCs possess the ability for perpetual self-renewal and proliferation, producing downstream progenitor cells that drive tumor growth. Studies of many cancer types have identified CSCs using specific markers, but it is still unclear as to where in the stem cell hierarchy these markers fall. This is compounded further by the presence of multiple GBM and glioblastoma cancer stem cell subtypes, making investigation and establishment of a universal treatment difficult. This review examines the current knowledge on the CSC markers SALL4, OCT-4, SOX2, STAT3, NANOG, c-Myc, KLF4, CD133, CD44, nestin, and glial fibrillary acidic protein, specifically focusing on their use and validity in GBM research and how they may be utilized for investigations into GBM’s cancer biology.
Highlights
Glioblastoma multiforme (GBM), a grade 4 astrocytoma, is the most aggressive form of glioma [1, 2] with the median survival of approximately 25 months following treatment [3]
This review aimed to provide a perspective on cancer stem cells (CSCs) markers SALL4, OCT-4, SOX2, STAT3, NANOG, c-Myc, Krüppel-like factor 4 (KLF4), CD133, CD44, nestin, and Glial fibrillary acidic protein (GFAP) reported in GBM, and attempt to place these markers in the context of the GBM CSC hierarchy, from the most primitive embryonic stem cells (ESCs) markers to the more mature
STAT3 has more generalized functions than the rest of the Signal transducers and activators of transcription (STAT) family and has been implicated in cell-cycle signaling, cell survival, and ESC self-renewal and pluripotency [122,123,124]. The latter activity has been proposed to be maintained via the leukemia inhibitory factor (LIF) pathway, in which LIF binds to its receptor and produces phosphorylation of STAT3 that subsequently translocates to the nucleus, triggering the expression of other ESC-associated proteins, such as KLF4, SOX2, SALL4, and c-Myc [62, 125, 126]
Summary
Amy Bradshaw , Agadha Wickremsekera1,2 , Swee T. Reviewed by: Kareem Zaghloul, National Institute of Neurological Disorders and Stroke, USA. Specialty section: This article was submitted to Neurosurgery, a section of the journal
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