Glioma is a type of mainstream brain tumor that has a short survival time even after surgery, radiation, and chemotherapy. A subgroup of gliomas called "glioma stem cells" plays an important role in tumor proliferation, tolerance to treatment, and tumor recurrence.
Recently, Dr. Ichiro Nakano from UAB and others, together with Dr. Maode Wang from Xi'an Jiaotong University, discovered a new molecular mechanism for the maintenance of glioma stem cells. Further, the authors found that the use of novel targeted molecular inhibitors has potential for the treatment of gliomas.
First, the authors found that a class of drugs called OTS167 is not ideal for clinical trials of malignant cancer, so they plan to study the underlying mechanisms by which gliomas develop tolerance to the drug. The authors found that a new class of molecular targets, NEK2, appears after gliomas are treated with OTS167. By targeting NEK2 with CMP3a, the growth of gliomas can be significantly inhibited, and this therapy combined with radiotherapy can provide a better tumor killing effect.
NEK2 is a class of previously studied kinase proteins. The researchers found that NEK2 is highly expressed in glioma stem cells, and NEK2 is important for the growth of gliomas in vitro. Mouse tumor model results also indicate that this protein is critical for the radiotherapy tolerance of tumor cells.
Through a series of experiments, the researchers found that NEK2 promotes tumor cell growth and tolerance mechanisms: they found that NEK2 protein can bind to a class of oncoprotein methyltransferase called EZH2, thereby protecting EZH2 from degradation. In turn, the self-renewal and survival of cancer stem cells are regulated.
Previous studies have found that EH2 is highly expressed in a variety of human cancers, and elevated EZH2 expression is accompanied by tumor deterioration and decreased therapeutic effects.
In another clinical trial, the authors found that the expression of NEK2 is closely related to EZH2 and is also related to the patient's health. The expression level of HEK2 is up-regulated in recurrent cancer cells. Therefore, the authors believe that NEK2 is an important class of factors that maintain the stability of glioma stem cells, and the specific inhibitor CMP3a can be a potential therapeutic drug.
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