In a study from VCU Massey Cancer Center, scientists found a cellular factor that drives the growth of deadly brain tumors could potentially serve as a novel target for disease treatment.
Gliomas are any cancer that starts in the glial cells of the nervous system and account for nearly one-third of all brain tumors.
The most aggressive type of glioma is called glioblastoma (GBM), which affects the brain and is virtually incurable.
The new study uncovered a previously unknown genetic process that could inform the development of novel treatment options for GBM.
The epidermal growth factor receptor (EGFR) signaling pathway has previously been shown to be highly active in the majority of GBMs.
Signaling pathways are like a cellular chain-of-command through which a string of proteins is triggered in a sequence to stimulate a specific cell function.
The irregular activation of certain pathways can often lead to the development of diseases, including cancer.
Previous research indicates that the EGFR pathway obstructs a natural process through which cells stop dividing called senescence, a mechanism that is critical in stunting the growth and spread of cancer cells.
Blocking the function of the EGFR pathway promotes senescence and helps prohibit tumor growth.
Through this new study, the team demonstrated that a specific protein called ubiquitin-specific protease 16 (USP16) regulates senescence and mitigates the growth of glioma cells.
They also identified a separate strand of long non-coding RNA—molecules that control gene activity—called lncEPAT that is activated through EGFR and is highly functional in GBM.
The findings suggest that lncEPAT acts as a genetic moderator allowing for EGFR to escape the antitumor role of USP16 and fuel cancer progression.
In preclinical models, Huang found that the depletion of lncEPAT increased the activity of USP16 and stifled GBM cell growth.
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The study was conducted by Suyun Huang et al and published in Science Advances.
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