8 research outputs found
Additional file 2 of Transcription factor AP2 enhances malignancy of non-small cell lung cancer through upregulation of USP22 gene expression
Additional file 1. Supplementary figures and tables
Supplementary Figures S1-S6 from G9a Promotes Invasion and Metastasis of Non–Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-κB Signaling Pathway
Figure S1. G9a silencing suppressed cell proliferation in A549 and H1299 NSCLCs Figure S2. Cell migration and invasion was suppressed in NSCLCs treated by G9a inhibitor UNC0638 Figure S3. G9a overexpression increased cell proliferation in NSCLCs Figure S4. FAK inhibitor attenuates the enhanced cell migration and invasion by G9a overexpression Figure S5. knockdown of G9a suppressed tumor metastasis in vivo. Figure S6. NF-kappa;B signaling pathway is independent of Wnt signaling pathway.</p
Figure S4 from Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma
Correlation between the levels of USP22 mRNA with that of ALDH1A3 mRNA in lung Adenocarcinoma tissues from TCGA portal</p
Figure S1 from Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma
Immunofluorescence of CD133 and USP22/H2Bub1</p
Figure S3 from Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma
Knockdown of USP22 in A549, H1299, and H838 lung cancer cells significantly down-regulated ALDH1A3 mRNA expression in these cells</p
Figure S5 from Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma
Correlation between the levels of CD133 (PROM1) mRNA with that of ALDH1A3 mRNA in lung adenocarcinoma tissues from TCGA portal</p
Figure S2 from Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma
USP22 knockdown with another USP22-shRNA</p
Genome-wide methylomic and transcriptomic analyses identify subtype-specific epigenetic signatures commonly dysregulated in glioma stem cells and glioblastoma
<p>Glioma stem cells (GSCs), a subpopulation of tumor cells, contribute to tumor heterogeneity and therapy resistance. Gene expression profiling classified glioblastoma (GBM) and GSCs into four transcriptomically-defined subtypes. Here, we determined the DNA methylation signatures in transcriptomically pre-classified GSC and GBM bulk tumors subtypes. We hypothesized that these DNA methylation signatures correlate with gene expression and are uniquely associated either with only GSCs or only GBM bulk tumors. Additional methylation signatures may be commonly associated with both GSCs and GBM bulk tumors, i.e., common to non-stem-like and stem-like tumor cell populations and correlating with the clinical prognosis of glioma patients. We analyzed Illumina 450K methylation array and expression data from a panel of 23 patient-derived GSCs. We referenced these results with The Cancer Genome Atlas (TCGA) GBM datasets to generate methylomic and transcriptomic signatures for GSCs and GBM bulk tumors of each transcriptomically pre-defined tumor subtype. Survival analyses were carried out for these signature genes using publicly available datasets, including from TCGA. We report that DNA methylation signatures in proneural and mesenchymal tumor subtypes are either unique to GSCs, unique to GBM bulk tumors, or common to both. Further, dysregulated DNA methylation correlates with gene expression and clinical prognoses. Additionally, many previously identified transcriptionally-regulated markers are also dysregulated due to DNA methylation. The subtype-specific DNA methylation signatures described in this study could be useful for refining GBM sub-classification, improving prognostic accuracy, and making therapeutic decisions.</p