Immortalized cell lines contain circadianclocks conducting transcriptional/translational rhythms in gene expressionwhereas metabolic rhythms can persist without transcription. Circadian rhythm disruptionby modern life may cause higher cancer risk; however, little is known aboutclock functioning in tumor cells. Here we evaluated glycerophospholipid (GPL)and redox metabolisms in cultures of glioblastoma T98G cells underproliferation (P) or partial arrest (A), synchronized with dexamethasone (100nM) (time 0) and collected at different times. In arrested cultures, mRNAs forclock-(Bmal1, Per1, Rev-erbα) and GPL enzyme genes, and 32P-GPL labeling exhibited circadianrhythmicity; oscillations were also found in the redox state/peroxiredoxinoxidation cycles. In proliferating cells, circadian rhythms of gene expressionwere lost or their periodicity shortened whereas the metabolic rhythms persistwith a similar or longer period to that observed under A Also, cell viabilitysignificantly changed over time after bortezomib (500 nM) treatment.Nevertheless, cell viability and redox state rhythms were altered when Bmal1 expression was knocked down by CRISPR/Cas 9 genomic editing technology.Results support that a metabolic clock operates in proliferative tumor cellsregardless the molecular clock; property that may confer tumor susceptibilityfor a time-dependent chemotherapy.