CA3 bridges dietary restriction to glioblastoma suppression and tumor progression as a key downstream effector.

Dietary restriction (DR) is recognized as a health-promoting, non-pharmacological intervention with demonstrated inhibitory effects on the initiation and progression of cancer. The molecular mechanisms underpinning DR's anticancer activity are pivotal, with documented evidence of its suppressive role across a spectrum of cancers. Glioblastoma multiforme (GBM) represents an aggressively malignant intracranial neoplasm, and despite incremental therapeutic and managerial advancements, the clinical outcomes remain suboptimal. Consequently, the discovery of novel molecular markers to augment diagnostic accuracy and therapeutic efficacy is imperative. Employing an array of bioinformatics strategies, we conducted an exhaustive analysis of molecules associated with DR, culminating in the identification of CA3 as a novel molecular marker for GBM. We evaluated its diagnostic and therapeutic potential within GBM. Our data indicate that the DR-associated molecule CA3 may exhibit correlations with multiple GBM phenotypes, including the immune contexture, with particular emphasis on the tumor's invasive and migratory capacities. Subsequent inquiries confirmed that modulating CA3 expression can effectively curb the genesis and progression of GBM. Our research substantiates that DR can mitigate the onset and development of GBM via the gene CA3, thereby validating a novel GBM marker and proposing a non-pharmacological interventional approach for this life-threatening condition.