Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic and Epigenomic Profiling of MYADM and RhoA Regulatory Networks in Metastatic Cancer Models

ABSTRACT: This dataset comprises bulk RNA-seq and ATAC-seq profiles across multiple human and murine cell lines with diverse metastatic potentials to investigate the role of MYADM and RhoA in cancer progression. RNA-seq samples include MYADM and RhoA knockdown in murine breast cancer cells (4T1), MYADM overexpression in human mammary epithelial cells (MCF10A), and metastatic progression models derived from human kidney (ACHN) and lung (CL1 series) cell lines. Additionally, transcriptomic data were collected from bone marrow-derived monocytes isolated from wild-type and MYADM whole-body knockout mice. ATAC-seq data were generated from selected RNA-seq matched samples to characterize chromatin accessibility changes associated with MYADM and RhoA perturbation. All cells were cultured under standard conditions. This dataset provides insights into transcriptional and epigenetic alterations during MYADM- and RhoA-mediated cancer metastasis.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE297013 | GEO | 2025/08/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human normal and RhoA immortal cells

Project description:Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably utilized immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMECs). We found that ectopic expression of wild-type RhoA as well as a constitutively-active RhoA mutant (G14V) in primary hMEC strains led to their immortalization and preneoplastic transformation. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well known Rho-effectors ,was also capable of immortalizing hMECs.Our results demonstrate that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked cellular transformation and breast cancer. Through microarray analysis, we want to identify genes and pathways linked to RhoA induced hMECs immortalization. Experiment Overall Design: 4 samples, in triplicate analyses per sample.

2008-10-26 | E-GEOD-12917 | biostudies-arrayexpress

Gene expression changes in gastric and colon cancer cell lines after RHOA knockdown.

Project description:RHOA is a recurrently mutated gene in diffuse-type gastric cancer, whose molecular influence in gastric cancer has not been well uncovered. We aimed to clarify the contribution of RHOA to pro-oncogenesis to improve the understanding of the role of RHOA as a therapeutic target. We performed microarray analysis after RHOA knockdown for HGC-27, AGS, CCK-81, and SW948.

2021-02-01 | GSE110237 | GEO

Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [scRNA-seq]

Project description:Biomechanical alterations contribute to the decreased regenerative capacity of hematopoietic stem cells (HSCs) upon aging. RhoA is a key regulator of mechanosignaling, but its role in mechanotransduction in stem cell aging remains unclear. Here we show that murine HSCs respond to increased nuclear envelope (NE) tension by inducing NE translocation of P-cPLA2, which cell-intrinsically activates RhoA. Aged HSCs experience physiologically higher intrinsic NE tension, but reducing RhoA activity lowers NE tension in aged HSCs. Feature image analysis of HSC nuclei reveals that chromatin remodeling is associated with RhoA inhibition, including restoration of youthful levels of the heterochromatin marker H3K9me2 and a decrease in chromatin accessibility and transcription at retrotransposons. Finally, we demonstrate that RhoA inhibition upregulates Klf4 expression and transcriptional activity, improving aged HSC regenerative capacity and lympho/myeloid skewing in vivo. Together, our data outline an intrinsic RhoA-dependent mechanosignaling axis, which can be pharmacologically targeted to restore aged stem cell function.

2025-08-29 | GSE269953 | GEO

Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [bulk ATAC-seq]

2025-08-29 | GSE233986 | GEO

Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [bulk RNA-seq]

2025-08-29 | GSE233985 | GEO

Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [bulk ATAC-seq confinement]

2025-08-29 | GSE269396 | GEO

Gene expression profile of normal and RhoA immortal cells

2008-09-26 | GSE12917 | GEO

Expression data from RhoA-null and wildtype keratinocytes

Project description:Using mice with a keratinocyte-restricted deletion of the RhoA gene, we explored its role in the regulation of gene expression in vivo and in vitro RNA was isolated from RhoA-null or wildtype keratinocytes, in two different conditions, freshly isolated (in vivo) or cultured (in vitro), using the RNeasy kit (Qiagen, Germany). Hybridization to GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA) was carried out at the Copenhagen University Hospital Microarray Center using standard protocols. 2 biological replicates were analyzed for each in vivo genotype (2 samples from RhoA-null, 2 from wildtype), while 3 replicates for each in vitro genotype.

2015-01-07 | E-GEOD-64714 | biostudies-arrayexpress

Second generation molecules targeting the oncogenic signal mediator, RHOA in gastric cancer

Project description:Previously, we designed pharmacologically optimized inhibitor RHOA, a major signaling hub in gastric cancer (GC), the fourth most common cause of death in the world. Here, based on that previous work, we perform the lead optimization and design new RHOA inhibitors for greater anti-GC potency. Two of these compounds, JK-206 and -312 inhibit cell viability and migration of GC cell lines. Furthermore, through our transcriptomics analysis of JK-206 treatment in GC cells, we revealed that pharmacologic inhibition of RHOA was associated with inhibition of mitogenic pathway, including BIRC5. Thus, RHOA→BIRC5 can be regarded as a new therapeutic strategy in GC, possibly regulating proliferation and migration in oncogenic mechanisms.

2022-03-24 | GSE188908 | GEO

Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [bulk ATAC-seq]

Project description:Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells [bulk ATAC-seq]

| PRJNA979159 | ENA