Research Paper Volume 10, Issue 12 pp 3957—3985

Integrated multi-omics characterization reveals a distinctive metabolic signature and the role of NDUFA4L2 in promoting angiogenesis, chemoresistance, and mitochondrial dysfunction in clear cell renal cell carcinoma

Figure 4. Immunofluorescence showing the increase in MitoTracker signal levels in ccRCC cells treated with small interfering RNA targeting NDUFA4L2 (siNDUFA4L2) compared to untreated cells (A). The autophagic marker LC3 is increased in ccRCC cells and co-localizes with the mitochondrial label MitoTracker. A line profile is shown (B). NDUFA4L2-silenced cancer cells show an increased superoxide radicals production (C), high levels of phospho-H2AX (C), a significant accumulation of 8-oxodG (D), and a reactive increased expression of the DNA repair enzyme OGG1 (D). NDUFA4L2 silencing increased the membrane potential in cancer cells, as shown by increased signals of the fluorescence probe TMRE (E).