Fig 2: NDUFA4L2 is involved in the survival and migration of non‐small cell lung cancer (NSCLC) in hypoxia. (a) NDUFA4L2 messenger RNA (mRNA) of human NSCLC tissue samples was measured by quantitative PCR. (b) Four pairs of tissue samples were randomly extracted and measured by Western blotting. (c) The results of quantitative analysis of NDUFA4L2 were significant. (d) The expression of NDUFA4L2 and HIF‐1α was measured by immunohistochemical staining. A high percentage of tumor cells and high staining intensity indicate high expression. Pneumocytes were the normal cells. (e) HIF‐1α and NDUFA4L2 protein levels in NSCLC cell lines were measured by Western blotting assays. (f–i) The results of quantitative analysis of NDUFA4L2 and HIF‐1α were significant. () Normoxia (NX), and () Hypoxia (HY). (j) Wound healing assays in NSCLC cell lines cultured in normoxia and hypoxia are shown. All data were analyzed as the mean ± standard deviation from at least three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 versus control. H, hours; NT, normal tissues; TT, tumor tissues.

Fig 3: Mitochondrial NDUFA4L2 was activated by HIF‐1α. Non‐small cell lung cancer (NSCLC) cell lines were cultured in hypoxic conditions. (a) DMOG promoted and 2‐ME inhibited NDUFA4L2 expression. (b,c) Western blotting assays showed that apoptosis of NSCLC cell lines was increased by 2‐ME and inhibited by DMOG. (d–i) The results of quantitative analysis of NDUFA4L2, HIF‐1α, and cleaved caspase‐3 (C‐caspase3) were significant. All data were analyzed as the mean ± standard deviation from at least three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 versus control. DMSO, dimethyl sulfoxide.