Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Super-enhancer-driven PPP1R15B/CReP, regulated by C/EBPβ and YY1, is oncogenic in multiple myeloma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267004 | GEO | 2024/06/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Super-enhancer-driven PPP1R15B/CReP, regulated by C/EBPβ and YY1, is oncogenic in multiple myeloma

Project description:We identified a novel super-enhance-driven oncogene PPP1R15B overexpressed in multiple myeloma as compared to normal plasma cells and B lymphoma cells. We used PPP1R15B specific shRNAs to study its function.

2024-06-25 | GSE213556 | GEO

Super-enhancer-driven PPP1R15B/CReP, regulated by C/EBPβ and YY1, is oncogenic in multiple myeloma [HiChIP II]

Project description:H3K27ac HiChIP analysis was performed in multiple myeloma cell lines and primary sample to analyze active chromatin-chromatin interactions in myeloma.

2024-06-25 | GSE267003 | GEO

Super-enhancer-driven PPP1R15B/CReP, regulated by C/EBPβ and YY1, is oncogenic in multiple myeloma [HiChIP I]

Project description:H3K27ac HiChIP analysis was performed in two multiple myeloma cell lines to analyze active chromatin-chromatin interactions in myeloma.

2024-06-25 | GSE214018 | GEO

CDK7 inhibition suppresses super-enhancer-linked oncogenic transcription in MYCN-driven cancer.

Project description:The MYC oncoproteins are thought to stimulate tumor cell growth and proliferation through amplification of gene transcription, a mechanism that has thwarted most efforts to inhibit MYC function as potential cancer therapy. Using a covalent inhibitor of cyclin-dependent kinase 7 (CDK7) to disrupt the transcription of amplified MYCN in neuroblastoma cells, we demonstrate downregulation of the oncoprotein with consequent massive suppression of MYCN-driven global transcriptional amplification. This response translated to significant tumor regression in a mouse model of high-risk neuroblastoma, without the introduction of systemic toxicity. The striking treatment selectivity of MYCN-overexpressing cells correlated with preferential downregulation of super-enhancer-associated genes, including MYCN and other known oncogenic drivers in neuroblastoma. These results indicate that CDK7 inhibition, by selectively targeting the mechanisms that promote global transcriptional amplification in tumor cells, may be useful therapy for cancers that are driven by MYC family oncoproteins.

| S-EPMC4243043 | biostudies-literature

Oncogenic HOXB8 is driven by MYC-regulated super-enhancer and potentiates colorectal cancer invasiveness via BACH1

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-04 | GSE121209 | GEO

Transcriptional heterogeneity overcomes super-enhancer disrupting drug combinations in multiple myeloma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-25 | GSE244003 | GEO

A multi-omic dissection of super-enhancer driven oncogenic gene expression programs in ovarian cancer.

Project description:The human genome contains regulatory elements, such as enhancers, that are often rewired by cancer cells for the activation of genes that promote tumorigenesis and resistance to therapy. This is especially true for cancers that have little or no known driver mutations within protein coding genes, such as ovarian cancer. Herein, we utilize an integrated set of genomic and epigenomic datasets to identify clinically relevant super-enhancers that are preferentially amplified in ovarian cancer patients. We systematically probe the top 86 super-enhancers, using CRISPR-interference and CRISPR-deletion assays coupled to RNA-sequencing, to nominate two salient super-enhancers that drive proliferation and migration of cancer cells. Utilizing Hi-C, we construct chromatin interaction maps that enable the annotation of direct target genes for these super-enhancers and confirm their activity specifically within the cancer cell compartment of human tumors using single-cell genomics data. Together, our multi-omic approach examines a number of fundamental questions about how regulatory information encoded into super-enhancers drives gene expression networks that underlie the biology of ovarian cancer.

| S-EPMC9307778 | biostudies-literature

Super-Enhancer Associated Five-Gene Risk Score Model Predicts Overall Survival in Multiple Myeloma Patients.

Project description:Multiple myeloma (MM) is a malignant plasma cell tumor with high heterogeneity, characterized by anemia, hypercalcemia, renal failure, and lytic bone lesions. Although various powerful prognostic factors and models have been exploited, the development of more accurate prognosis and treatment for MM patients is still facing many challenges. Given the essential roles of super-enhancer (SE) associated genes in the tumorigenesis of MM, we tried to initially screen and identify the significant prognostic factors from SE associated genes in MM by the least absolute shrinkage and selection operator (Lasso) penalized Cox regression, univariate and multivariate Cox regression analysis using GSE24080 and GSE9782 datasets. Risk score model of five genes including CSGALNACT1, FAM53B, TAPBPL, REPIN1, and DDX11, was further constructed and the Kaplan-Meier (K-M) curves showed that the low-risk group seems to have better clinical outcome of survival compared to the high-risk group. Time-dependent receiver operating characteristic (ROC) curves presented the favorable performance of the model. An interactive nomogram consisting of the five-gene risk group and eleven clinical traits was established and identified by calibration curves. Therefore, the risk score model of SE associated five genes developed here could be used to predict the prognosis of MM patients, which may assist the clinical treatment of MM patients in the future.

| S-EPMC7744621 | biostudies-literature

Non-overlapping Control of Transcriptome by Promoter- and Super-Enhancer-Associated Dependencies in Multiple Myeloma.

Project description:The relationship between promoter proximal transcription factor-associated gene expression and super-enhancer-driven transcriptional programs are not well defined. However, their distinct genomic occupancy suggests a mechanism for specific and separable gene control. We explored the transcriptional and functional interrelationship between E2F transcription factors and BET transcriptional co-activators in multiple myeloma. We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells. Global chromatin analysis reveals distinct regulatory axes for E2F and BETs, with E2F predominantly localized to active gene promoters of growth and/or proliferation genes and BETs disproportionately at enhancer-regulated tissue-specific genes. These two separate gene regulatory axes can be simultaneously targeted to impair the myeloma proliferative program, providing an important molecular mechanism for combination therapy. This study therefore suggests a sequestered cellular functional control that may be perturbed in cancer with potential for development of a promising therapeutic strategy.

| S-EPMC6407615 | biostudies-literature

Super-enhancer profiling combined with CDK7 inhibition-transcripts identifies novel oncogenes of multiple myeloma.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-16 | GSE145938 | GEO