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 8. Immunoblot analysis of Caki-2 cells cultured under normoxic (21% O2) or hypoxic (1% O2) conditions for 18 hr and probed against NDUFA4L2, LC3, and TOM20 antibodies. Beta actin was used as a loading control (A). The silencing of NDUFA4L2 impairs cancer cell proliferation, inhibits the autophagic machine, and increases the levels of the mitochondrial protein TOM20, especially in hypoxic conditions (B). Cell proliferation was restored when NDUFA4L2-silenced cells were pre-treated with ascorbic acid 2-phosphate (AA2P) (B).