APE1 regulates a vast majority of genes by acting as a transcriptional co-activator or as a co-repressor. It is overexpressed in diverse cancer tissues and is associated with their drug resistance. It is essential for cell proliferation. APE1 is post-translationally acetylated by HAT p300 at its N-terminal Lys 6 and 7 residues. We examined APE1 and its acetylation-dependent gene expression profile of lung cancer cells which would contribute to sustained proliferation of lung cancer cells.
Regulation of limited N-terminal proteolysis of APE1 in tumor via acetylation and its role in cell proliferation.
Cell line
View SamplesTranscriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.
Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesAnalysis of T3 response in KCL034, iKCL004 and BJ cells at gene expression level. Results provide information of the T3 response in different lines.
No associated publication
Cell line, Treatment
View SamplesThis study was undertaken to compare efficacy of MJC13 and the classic AR antagonist flutamide. Both compounds modulate endogenous AR target gene expression in Prostate cancer cells in a similar fashion despite different mechanisms of action.
No associated publication
Cell line
View SamplesTAMs play an important role in MM drug resistance and progression. To determine the mechanisms about how tumor microenvironment regulate the generation of TAMs from normal MΦs in vitro and in vivo. We generated TAMs in vitro by tumor cells-MΦs coculture from CD36 WT and KO mice bone marrow cells. Total RNAs of 2 x 106 MΦs and TAMs were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Gene Expression and Genotyping Facility at Case Western Reserve University (Cleveland, OH) for RNA-seq followed by data analysis.
Enhanced Lipid Accumulation and Metabolism Are Required for the Differentiation and Activation of Tumor-Associated Macrophages.
No sample metadata fields
View SamplesThe enumeration of EpCAM-positive circulating tumor cells (CTCs) has allowed clinicians to estimate the overall metastatic burden in breast cancer patients. However, a thorough understanding of CTCs associated with breast cancer brain metastasis (BCBM) is necessary for early identification and evaluation of treatment response to BCBM. In this study, we report that BCBM CTCs are enriched in a distinct sub-population of cells identifiable by their biomarker expression and mutational content.
Molecular characterization of breast cancer CTCs associated with brain metastasis.
Sex
View SamplesTo determine the global transcriptomic changes induced by treatment with the Beta Catenin antagonist BC2059 in AML cells
No associated publication
Specimen part, Cell line
View SamplesMacophage migration inhibitor (MIF) is important for MM resistance to proteasome inhibitors. To determine what signalling pathways are affected by MIF in MM cells, we established MIF-KO MM.1S and ARP-1 MM cell lines. Total RNAs of 2 x 106 CTR-KO and MIF-KO MM cells were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Gene Expression and Genotyping Facility at Case Western Reserve University (Cleveland, OH) for RNA-seq followed by data analysis.
MIF as a biomarker and therapeutic target for overcoming resistance to proteasome inhibitors in human myeloma.
Specimen part, Cell line
View SamplesThe BET (bromodomain and extra terminal) protein family members including BRD4 bind to acetylated lysines on histones and regulate the expression of important oncogenes, e.g., MYC and BCL2. Here we demonstrate the sensitizing effects of the histone hyperacetylation inducing pan-histone deacetylase inhibitor (HDI) panobinostat (PS) on human AML blast progenitor cells (BPCs) to the BET protein inhibitor JQ1. Treatment with JQ1 but not its inactive enantiomer (R-JQ1) was highly lethal against AML BPCs expressing mutant NPM1c+ with or without co-expression of FLT3-ITD, or AML expressing MLL fusion oncoprotein. JQ1 treatment reduced binding of BRD4 and RNA polymerase II to the DNA of MYC and BCL2, and reduced their levels in the AML cells. Co-treatment with JQ1 and the HDAC inhibitor panobinostat (PS) synergistically induced apoptosis of the AML BPCs, but not of normal CD34+ hematopoietic progenitor cells. This was associated with greater attenuation of MYC and BCL2, while increasing p21, BIM and cleaved PARP levels in the AML BPCs. Co-treatment with JQ1 and PS significantly improved the survival of the NOD/SCID mice engrafted with OCI-AML3 or MOLM13 cells (p < 0.01). These findings highlight co-treatment with a BRD4 antagonist and an HDI as a potentially efficacious therapy of AML.
Highly active combination of BRD4 antagonist and histone deacetylase inhibitor against human acute myelogenous leukemia cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway.
Specimen part
View Samples