Knockdown of Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Treatment Modulate Similar Macromolecular and Metabolic Changes in HeLa Cells

Background/aim: Despite great progress in complex gene regulatory mechanisms the dynamic tumor microenvironment, potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) a cisplatin inducible lncRNA whose knockdown modulates morphology. However, its effect on unknown. The aim this study examine metabolic changes modulated by and DR5-AS HeLa cells. Materials methods: We used as universal therapeutic drug modulate cervix then examined extent Fourier transform infrared spectroscopy (FTIR). also performed transcriptomics analyses generating new RNA-seq data with total isolated from cisplatin-treated Then, we compared cisplatin-mediated macromolecular those mediated knockdown. Results: Cisplatin treatment caused unsaturated fatty acid lipid-to-protein ratios glycogen content. These observations altered cellular were supported analyses. FTIR have revealed that causes 20.9% elevation lipid/protein ratio 76.6% decrease lipid peroxidation. Furthermore, detected 3.42% increase chain length aliphatic lipids, higher content RNA, lower amount indicating relatively activity Interestingly, observed similar expression pattern under Conclusion: results suggest appears account for fraction