Midkine signaling maintains the self-renewal and tumorigenic capacity of glioma initiating cells

Beyond glucose: alternative sources of energy in glioblastoma

“…The addition of TMZ augmented this process to further enhance glioma apoptosis and showed an increase in cell death when compared to the Rapa and chloroquine combination therapy. The efficacy of therapies such as TMZ, rapa, and chloroquine may be further augmented through combination therapies targeting the midkine (MDK) signaling axis 62 . MDK is a neurotrophic factor that promotes the senescence of glioma initiating cells (GICs) through inhibiting autophagic degradation of the transcription factor SOX9 62 .…”

“…The efficacy of therapies such as TMZ, rapa, and chloroquine may be further augmented through combination therapies targeting the midkine (MDK) signaling axis 62 . MDK is a neurotrophic factor that promotes the senescence of glioma initiating cells (GICs) through inhibiting autophagic degradation of the transcription factor SOX9 62 . Inhibition of the MDK signaling axis was shown to decrease the self-renewal capacity of GBM cells, particularly when combined with TMZ 62 .…”

“…MDK is a neurotrophic factor that promotes the senescence of glioma initiating cells (GICs) through inhibiting autophagic degradation of the transcription factor SOX9 62 . Inhibition of the MDK signaling axis was shown to decrease the self-renewal capacity of GBM cells, particularly when combined with TMZ 62 . Promising targets in autophagy and other areas of tumor metabolism are continually being identified.…”

Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases

“…Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase of the Class XVI that has been found to be implicated in multiple cancers through aberrant activation due to point mutations, overexpression, or a diversity of translocations giving rise to fusion proteins [99]. Studies in ALK+ anaplastic large cell lymphoma showed that treatment with the tyrosine kinase inhibitor crizotinib induced autophagy and that combination of ALK inhibition with Bcl-2 depletion induced autophagy and cell death [100,101], and autophagy induction was also found upon ALK inhibition in glioblastoma [102]. Aberrant RTK signaling is also involved in hepatocellular carcinoma (HCC), and RTK inhibitor sorafenib is used for therapy and was shown to induce autophagy in multiple systems [103].…”

Extracellular vesicles derived from hypoxic glioma stem-like cells confer temozolomide resistance on glioblastoma by delivering miR-30b-3p

“…Temozolomide (TMZ) is used as first-line chemotherapy for GBM treatment. However, glioma stem-like cells (GSCs), a subset of cancer cells capable of self-renewal 4 - 6 , limit GBMs' effective treatment due to their therapeutic resistance 7 , 8 . The generation and maintenance of GSCs require a supportive niche.…”