Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of lncRNA LINC00094 (SERLOC)

ABSTRACT: Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Long non-coding RNAs (lncRNAs) are involved in various biological processes, and their role in cancer progression is emerging. Whole transcriptome analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) revealed overexpression of long intergenic ncRNA (LINC00094) in cSCC cells (GSE66412). We wanted to futher study the RNA expression profile of LINC00094 knockdown cSCC cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205981 | GEO | 2022/08/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-Seq analysis of cSCC cells after siRNA-induced gene knockdown of lncRNA PRECSIT

Project description:Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Long non-coding RNAs (lncRNAs) are involved in various biological processes, and their role in cancer progression is emerging. Whole transcriptome analysis of cSCC cell lines (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) revealed overexpression of long intergenic ncRNA (LINC00346) in cSCC cells (GSE66412). We wanted to futher study the RNA expression profile of LINC00346 knockdown cSCC cells. Based on our observations, LINC00346 was named PRECSIT (p53 regulated carcinoma-associated STAT3-activating long intergenic non-protein coding transcript).

2019-10-16 | GSE138232 | GEO

RNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of AIM2.

2017-08-18 | GSE94270 | GEO

Long Non-coding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity

Project description:Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Long non-coding RNAs (lncRNAs) are involved in various biological processes, and their role in cancer progression is emerging. Whole transcriptome analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells (GSE66412). We wanted to futher study the RNA expression profile of LINC00162 knockdown cSCC cells. Based on our observations, LINC00162 was named PICSAR (P38 Inhibited Cutaneous Squamous cell carcinoma Associated lincRNA).

2016-08-31 | GSE77950 | GEO

RNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of C1s.

Project description:Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Chronic inflammation has been recognized as a risk factor for cSCC and inflammation is a typical feature in the progression of premalignant actinic keratosis lesions to invasive and metastatic cSCC. The complement system is an important part of innate immunity, and activation of complement is detected in the microenvironment of tumors and has been considered a host defense mechanism against cancer cells. The complement cascade can be activated via three distinct pathways, namely the classic, lectin, or alternative pathways, which all lead to activation of lytic pathway and formation of the membrane attack complex, a pore-like structure on the target cell membrane resulting in the lysis of the target cell. The classical pathway of complement is typically activated by binding of C1 complex to antibodies bound to their target antigens. The C1 complex consists of six subcomponents of C1q, each with a collagenous triple helix of subunits C1qA, C1qB, and C1qC chains and two copies of serine proteases C1r and C1s subunits each. Whole transcriptome analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) and oligonucleotide array-based expression analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=5) revealed overexpression of C1s in cSCC cells (GSE66412 and GSE66368, respectively). Inthis respect, we have wanted to futher study the RNA expression profile of C1s knockdown cSCC cells.

2019-10-22 | GSE121017 | GEO

mRNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of CFI.

Project description:Keratinocyte carcinomas (BCC and cSCC) are the most common cancers worldwide. cSCC is considered as the most prevalent metastatic skin malignancy and its incidence is increasing globally. The complement system is a fundamental part of the host immune defense. It is composed of three distinct pathways (classical, alternative and lectin) that get activated sequentially. However, the process of complement activation is rigorously regulated by a series of soluble and membrane-bound inhibitor proteins that protect the host cells from lytic damage. One of these soluble negative regulators is complement factor I (CFI) which is an 88 kDa serine protease that hampers all three complement pathways through blockade of C3- and C5- convertases by cleaving C3b and C4b. Oligonucleotide array (Affymetrix)-based analysis of normal human epidermal keratinocytes (NHEKs; n=5), primary (Prim. cSCC; n=5) and metastatic (Met. cSCC; n=3) cSCC cell lines as well as next-generation-sequencing (SOLiD) based transcriptome profiling of NHEKs (n=4), primary (Prim. cSCC; n=5) and metastatic (Met. cSCC; n=3) cSCC cell lines revealed marked overexpression of CFI in cSCC cells compared to NHEKs (GSE66368 and GSE66412 respectively). Furthermore, we have previously shown that knockdown of CFI inhibits proliferation and migration of cSCC cells and potently impedes growth of cSCC xenograft tumors in vivo. In these respects, we intended to further investigate the functional role and molecular mechanism of CFI in cSCC progression via analyzing the mRNA expression profile of CFI in cSCC cells.

2021-05-19 | GSE166421 | GEO

mRNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of C1r.

Project description:Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Chronic inflammation has been recognized as a risk factor for cSCC and inflammation is a typical feature in the progression of premalignant actinic keratosis lesions to invasive and metastatic cSCC. The complement system is an important part of innate immunity, and activation of complement is detected in the microenvironment of tumors and has been considered a host defense mechanism against cancer cells. The complement cascade can be activated via three distinct pathways, namely the classic, lectin, or alternative pathways, which all lead to activation of lytic pathway and formation of the membrane attack complex, a pore-like structure on the target cell membrane resulting in the lysis of the target cell. The classical pathway of complement is typically activated by binding of C1 complex to antibodies bound to their target antigens. The C1 complex consists of six subcomponents of C1q, each with a collagenous triple helix of subunits C1qA, C1qB, and C1qC chains and two copies of serine proteases C1r and C1s subunits each. Whole transcriptome analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) and oligonucleotide array-based expression analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=5) revealed overexpression of C1r in cSCC cells (GSE66412 and GSE66368, respectively). Previously it has been shown that knockdown of C1r promotes apoptosis of cSCC cells and significantly suppresses growth and vascularization of human cSCC xenograft tumors in vivo (Riihilä et al. Br J Dermatol 2020; 182:658-670). In this respect, we have studied the RNA expression profile of cSCC cells after C1r knockdown.

2021-11-17 | GSE174626 | GEO

RNA-Seq whole transcriptome analysis of normal human epidermal keratinocytes and cutaneous squamous cell carcinoma cell lines.

Project description:The incidence of keratinocyte-derived skin cancer, cutaneous squamous cell carcinoma (cSCC) is increasing worldwide making it the second most common metastatic skin cancer. In this project we used SOLiD next generation sequencing to characterize gene expression profiles in normal human epidermal keratinocytes (NHEKs) and cSCC cell lines. Total RNAs from normal human epidermal keratinocytes (NHEKs) (n=4) and cSCC cell lines (n=8) were extracted. The samples were sequenced using SOLiD next generation sequencing.

2015-08-27 | E-GEOD-66412 | biostudies-arrayexpress

RNA-Seq of human cutaneous squamous cell carcinoma cell lines and normal human epidermal keratinocytes.

2024-08-01 | GSE252347 | GEO

RNA-Seq whole transcriptome analysis of normal human epidermal keratinocytes and cutaneous squamous cell carcinoma cell lines.

2015-08-27 | GSE66412 | GEO

Proteomics study of skin tissues from RDEB cSCC, low-risk cSCC and metastasizing cSCC

Project description:Cutaneous squamous cell carcinoma (cSCC) is the leading cause of death in recessive dystrophic epidermolysis bullosa (RDEB) patients but remains poorly studied on a proteomic level. We aim to characterize the RDEB-SCC proteome by comparing it to the proteomes of UV-light induced cSCC of non-aggressive and aggressive behavior with which RDEB cSCC share either the well-differentiated morphology or the aggressive behavior, respectively. We applied a direct trypsinization protocol using an acid labile surfactant and label-free quantitation to study formalin-fixed, paraffin-embedded tissues from patients with RDEB cSCC (n=6), low-risk cSCC (n=5) and metastasizing cSCC (n=13) by liquid chromatography tandem-mass spectrometry.

2017-11-27 | PXD006914 | Pride

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