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MAPK pathway: Potential role in glioblastoma multiforme

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ELSEVIER
DOI: 10.1016/j.inat.2020.100901

Keywords

Glioblastoma multiforme; Brain tumor; Mitogen-activated protein kinase; Epidermal growth factor receptor; Tumor cells

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Research has shown that the MAPK signaling pathway plays a crucial role in GBM, affecting cell proliferation and survival. Targeting specific factors responsible for regulating the MAPK pathway can disrupt major tumor cell functions, including cell survival and proliferation.
Glioblastoma multiforme (GBM) is one of the most aggressive and damaging tumors of the brain. For successful therapy of GBM exact pathways need to be explored for developing effective targeted chemotherapeutic agents. MAPK signaling pathway components are expressed in several regions of the brain and results in excess overlapping expression pattern (except MEK2 pattern, which is totally absent) during non-pathological conditions. MAPK signaling pathway plays a key role in various cancers including GBM by hyperactivation and it has been concerned in various tumorigenic progressions like migration, proliferation, and survival. It has been reported that MAPK pathway signaling plays a key role in the co-activation of cell proliferation and CREB, a vital regulator of cyclin-D1 expression cell in GBM cells. Targeting to specific factors responsible for regulating MAPK pathway will interrupt the major tumor cell functions including survival and proliferation of cells. The major therapeutic strategies of the current GBM therapy is to increase the survivor rate of GBM patients. Further study in this area is necessary to explore the developmental cell-type specific effects of MAPK activation, and to investigate the possible link to a cell of origin for GBM. In this editorial, focus is to highlight the key role of the MAPK signaling pathway in GBM.

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