Midkine in Glioblastoma with the Modulator Role Switching Autophagy to Cell Death or Cell Survival

Glioblastoma (GBM) is the most common and lethal brain tumor. Characterization of GBM with poor prognosis although new treatment modalities hasn’t been changed up to date. New molecular targets in order to overcome resistance and recurrence are needed. Autophagy, a self-catabolic process, has two converse role in tumorigenesis, acting both as a tumor suppressor and a protector of cancer cell survival, tumor dormancy, progression, and therapeutic resistance. Autophagy with its dual role become target of cancer therapy. Midkine (MK), a growth factor with cytokine activity, is expressed highly during embryogenesis, but interestingly, MK is not detectable in healthy adults and only re-appears in the body as a part of the pathogenesis of diseases such as cancer. MK promotes proliferation, migration, anti-apoptotic manner, mitogenesis, transforming, and angiogenesis in various cells. In the central nervous system. High MK expression correlates with the progression of human astrocytomas, MK mRNA and protein expression levels were higher in high-grade astrocytomas as GBMs than in low-grade astrocytomas. MK correlates with the poor prognosis of GBM. This review is focused on the relationship between MK and autophagy in GBM and GBM treatment and pro­mising usage of MK in order to switch autophagy to cell death.