Additional file 2 of Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription
Abstract
Supplementary Material 2: Supplementary Fig. S2. Cisplatin-resistant cells exhibit enhanced mitochondrial RNA synthesis without changes in RNA stability. (A-F) RNA synthesis assays measuring the relative accumulation of newly synthesized transcripts in parental and cisplatin-resistant (CisR) HeLa cells at an initial (T0) and 2-hour (T1) time point. The analysis includes mtDNA-encoded genes (MT-ND1, MT-ND5, MT-CO1, MT-CYB, and MT-ATP6) and the nuclear-encoded 18 S rRNA control. (G-L) RNA decay assays measuring the stability of the same transcripts in parental and CisR cells following transcription inhibition. RNA levels were measured immediately (T0) and 24 h (T1) after inhibitor treatment. Data are presented as mean ± SD. Statistical significance was determined using Student’s t-test: *p < 0.05, **p < 0.01, ***p < 0.001, ns: not significant
Fields of Study & Subjects
Mitochondrial Function and Pathology
Cancer
Hypoxia
and Metabolism
Lipids
Publication details
- Journal / source
- Figshare
- Publication date
- 1 January 2026
- Language
- EN