Acetylation modification in malignant progression and therapeutic resistance of gliomas

Gliomas are the most common and aggressive primary malignant tumors of the central nervous system, characterized by diffuse infiltration, rapid proliferation and dismal prognosis. Despite advances in multimodal treatments, including surgical resection, radiotherapy and targeted therapies, clinical outcomes remain unsatisfactory owing to the inevitable development of therapeutic resistance. Protein acetylation, a key post-translational modification dynamically regulated by lysine acetyltransferases and deacetylases, plays a central role in governing chromatin organization, transcriptional regulation, protein stability and signal transduction. Increasing evidence indicates that aberrant acetylation critically contributes to glioma malignant progression and treatment resistance by modulating essential cellular processes, including proliferation, apoptosis, invasion, metabolic reprogramming, DNA damage repair, immune evasion and cancer stemness. This review systematically summarizes recent advances in understanding the roles of both histone and non-histone acetylation in glioma biology, with particular emphasis on their involvement in resistance to chemotherapy and radiotherapy. Collectively, this review underscores acetylation as a pivotal epigenetic mechanism driving glioma aggressiveness and therapeutic resistance and provides mechanistic insights and a conceptual framework for the development of more effective and precise therapeutic strategies.