Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRKCQ-dependent transcriptome in MyLa and HuT 78 cells

ABSTRACT: Transcriptional profiling controlled by PRKCQ of human CTCL cell lines MyLa and HuT 78 comparing cells transfected with non-targeting control with shPRKCQ cells at resting conditions and by TPA. The objective was to explore the role of PRKCQ in the pathogenesis of cutaneous T-cell lymphoma(CTCL).

ORGANISM(S): Homo sapiens

PROVIDER: GSE157442 | GEO | 2020/09/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PRKCQ-dependent transcriptome in MyLa and HuT 78 cells

Project description:PRKCQ-dependent transcriptome in MyLa and HuT 78 cells

| PRJNA661313 | ENA

Gene expression profiling of mycosis fungoides with and without LCT as well as CTCL cell lines via PEG10 knockdown and overexpression by RNA-seq

Project description:Mycosis fungoides (MF), the most common subtype of cutaneous T-cell lymphoma (CTCL), may undergo large-cell transformation (LCT), which is related to aggressive clinical courses and resistance to conventional treatments. However, the mechanisms of LCT remain largely unknown.We performed RNA-seq on biopsied specimens isolated from 26 MF-LCT patients and 23 MF-NLCT patients to decipher the mechanisms underlying LCT. We found PEG10 was overexpressed in MF-LCT compared with MF -NLCT cases. In order to explore the function of PEG10 in the pathogenesis of MF, transcriptome sequencing was performed among HH cells transfected with shRNAs targeting PEG10 (shPEG10) and scrambled shRNA(sh0) , Myla cells transfected with empty vetors(vec) and PEG10 expression vectors ( RF1b, RF1b/2, RF1b/2+CNF) to investigate genes regulated by PEG10 in CTCL cells .

2021-12-25 | GSE168508 | GEO

CTCL cell line H9:vehicle control vs.ShBCL11B

Project description:Transcriptional profiling of human CTCL cell line H9 comparing cells transfected with vehicle control with ShBCL11B cells. Previous study have shown the involvements of BCL11b/BCL11B in T cell development and hematopoietic malignancies of T-cell origin. Objective was to explore the action of BCL11B in the pathogenesis of cutaneous T-cell lymphoma(CTCL).

2019-12-17 | GSE90616 | GEO

Oncogenic role of TOX in CTCL

2014-04-29 | GSE57122 | GEO

Gene expression profiling of CTCL patient-derived cell lines after GTSF1 knockdown

Project description:In CTCL, the ectopic expression of Gametocyte Specific Factor 1 (GTSF1) has emerged as a potential prognostic biomarker. High expression of GTSF1 has been associated with a worse overall prognosis for patients. However, the contribution of GTSF1 to CTCL carcinogenesis remains unknown. We performed a shRNA mediated silencing of GTSF1 in three cell lines representing the most common variants of CTCL: Mac2A, representative of primary cutaneous Anaplastic Large Cell Lymphoma; MyLa 2000, representative of Mycosis Fungoides; and SZ4, representative of Sézary Syndrome. The three cell lines showed different gene expression profiles, signaling the different clinical behaviors of each variant. In Mac2A, silencing of GTSF1 in CTCL led to T cell activation and production of IFNγ and TNFα. This suugests that GTSF1 contributes to carcinogenesis by partially modifying the effector-memory phenotype of the malignant T cells.

2024-07-02 | GSE270818 | GEO

Oncogenic role of TOX in CTCL

Project description:TOX is a nuclear factor essential for the development of CD4+ T cells in the thymus. TOX is found to be aberrantly up-regulated in the skin biopsies and in the blood CD4+ T cells of cutaneous T cell lymphoma. The goal of this study is to identify potential transcriptional targets of TOX in CTCL by comparison between TOX shRNA transfected CTCL cells (Hut78 and HH) and control CTCL cells. Two color experiment. Lentivirus transduced control vector vs. TOX shRNA vectors on Hut78 and HH cell lines. Biological replicates: 3 control replicates, 3 shRNA tansduced replicates for each cell line.

2014-04-29 | E-GEOD-57122 | biostudies-arrayexpress

Identification of genes that regulated by IRF4 in human cutaneous T cell lymphoma HuT-102 cells

Project description:The microarray analysis showed an interesting up-regulation in the set of genes controlling the development of Th1, mainly IFN-gamma, and other type 1 interferon response genes including CXCL10 in IRF4 knocked-down HuT-102 cells. HuT-102 cells, a human cutaneous T cell lymphoma, were transiently transfected with siRNAs against human IRF4 or firefly luciferase. Cells were incubated for 60 h at 37 centigrade. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChipÂ® system with a Human Genome U133-plus 2.0 array for analysis of over 47,000 transcripts. Sample preparation for array hybridization was carried out as described in the manufacturerâs instructions.

2010-06-08 | E-GEOD-22036 | biostudies-arrayexpress

PCALCL cell line Mac1:vehicle control vs.shEZH2

Project description:Transcriptional profiling of human PCALCL cell line Mac1 comparing cells transfected with vehicle control with shEZH2 cells. Previous study have shown the involvements of EZH2 in T cell development and hematopoietic malignancies of T-cell origin. Objective was to explore the action of EZH2 in the pathogenesis of cutaneous T-cell lymphoma(CTCL).

2018-03-31 | GSE96742 | GEO

Transcription profiling of Hut 78 cells (Sezary sndrome) with a stable knockdown of AHI-1 expression to identify mediators of the AHI-1.

Project description:AHI-1 is an oncogene often targeted by provirus insertional mutagenesis in murine leukemias and lymphomas. Aberrant expression of human AHI-1 occurs in cutaneous T-cell lymphoma (CTCL) cells and in CD4+CD7- Sezary cells from patients with Sezary syndrome (SS). Stable knockdown of AHI-1 using retroviral-mediated RNA interference in CTCL cells inhibits their transforming activity in vitro and in vivo. To identify genes involved in AHI-1-mediated transformation, microarray analysis was performed to identify differentially expressed genes in AHI-1 suppressed CTCL cells. Fifteen up-regulated and six down-regulated genes were identified and confirmed by Q-RT-PCR. Seven were further confirmed in a microarray analysis of CD4+CD7- Sezary cells from SS patients. HCK and BIN1 emerged as new candidate cooperative genes, with differential protein expression which correlates with observed transcript changes. Interestingly, changes in HCK phosphorylation and biological response to its inhibitor, dasatinib, were observed in AHI-1 suppressed or overexpressed cells. The tumor suppressor BIN1 physically interacts with MYC in CTCL cells, which also exhibit differential MYC protein expression. In addition, aberrant expression of alternative splicing forms of BIN1 was observed in primary and transformed CTCL cells. These findings indicate that HCK and BIN1 may play critical roles in AHI-1-mediated leukemic transformation of human CTCL cells. Experiment Overall Design: Two groups, each with two subgroups, subgroups having 2 or 3 replicates each

2009-02-21 | E-GEOD-14746 | biostudies-arrayexpress

Gene expression profiling of CTCL cell line Hut78 via IKZF2 knockdown by RNA-seq

Project description:IKZF2 is an important nuclear matrix protein and plays a pivotal role in T cell development and differentiation, while its expression and function in Cutaneous T cell lymphoma (CTCL) remain ambiguous. Our study aimed to investigate the expression pattern, biological function of IKZF2 in a large clinical cohort. IKZF2 is specifically over-expressed in malignant T cells with MF tumor-stage. In order to explore the function of IKZF2 in the pathogenesis of CTCL, transcriptome sequencing was performed among Hut78 cells transfected with shRNAs targeting IKZF2 (shIKZF2) and scrambled shRNA(sh0) to investigate genes regulated by IKZF2 in CTCL cells .

2022-02-28 | GSE179433 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data