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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: IκBα targeting promotes oxidative stress-dependent cell death

Fig. 1

Identification of NFKBIA amplification in cancers. a and b NFΚBIA gene amplification samples analyzed by the TCGA database. Lung Adenocarcinoma (LUAD), Head and Neck Carcinoma (HEAD_NECK), Esophageal Cancer (ESOPH), Lung Squamous Carcinoma (LUSC), Breast Carcinoma (BRCA), Uterine Corpus Endometrioid Carcinoma (UCEC), Glioblastoma Multiforme (GBM), Acute Myeloid Leukemia (LAML), Ovarian Cancer (OVARIAN), Bladder Urothelial Carcinoma (BLCA), Colorectal Adenocarcinoma (COAD), Kidney Renal Clear Cell Carcinoma (KIRC), Rectal Adenocarcinoma (READ). c NFΚBIA mRNA expression levels analyzed by the TCGA database in Lung Adenocarcinoma, head and neck cancer, Lung Squamous Carcinoma and Esophageal Cancer. d Non-thresholded chromosome 14 LUAD tumors copy number profile. Positive y-axis values indicate prevalent amplification, negative values prevalent deletion. The position of a subset of chromosome 14 genes is shown in the lower part of the figure. NFΚBIA is shown in red. e LUAD dataset NFΚBIA copy number density heatmap. The contour of the transcriptional region characterized by the presence of high density NFΚBIA amplification is highlighted by the presence of grey arrows (f). g Representative IκBα IHC staining on lung biopsy patients. Graph showing the IHC quantification of IκBα expression in lung cancer patients. h Immunoblotting of IκBα and vinculin in lung cancer cells line. i Gene set enrichment analysis plot analyzed by the TCGA database of NF-κB signaling, apoptotic hallmarks (j), oxidative phosphorylation (k) and reactive oxygen species (l)

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