Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

ABSTRACT: MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

PROVIDER: PRJNA693873 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13501100_1.fastq.gz	Fastqsanger.gz
	SRR13501100_2.fastq.gz	Fastqsanger.gz
	SRR13501101_1.fastq.gz	Fastqsanger.gz
	SRR13501101_2.fastq.gz	Fastqsanger.gz
	SRR13501102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

Project description:MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

2021-05-01 | GSE165286 | GEO

MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

Project description:MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

| PRJNA698613 | ENA

MicroRNA-138 suppresses glioblastoma proliferation through downregulation of CD44.

Project description:Tumor suppressive microRNAs (miRNAs) are increasingly implicated in the development of anti-tumor therapy by reprogramming gene network that are aberrantly regulated in cancer cells. This study aimed to determine the therapeutic potential of putative tumor suppressive miRNA, miR-138, against glioblastoma (GBM). Whole transcriptome and miRNA expression profiling analyses on human GBM patient tissues identified miR-138 as one of the significantly downregulated miRNAs with an inverse correlation with CD44 expression. Transient overexpression of miR-138 in GBM cells inhibited cell proliferation, cell cycle, migration, and wound healing capability. We unveiled that miR-138 negatively regulates the expression of CD44 by directly binding to the 3' UTR of CD44. CD44 inhibition by miR-138 resulted in an inhibition of glioblastoma cell proliferation in vitro through cell cycle arrest as evidenced by a significant induction of p27 and its translocation into nucleus. Ectopic expression of miR-138 also increased survival rates in mice that had an intracranial xenograft tumor derived from human patient-derived primary GBM cells. In conclusion, we demonstrated a therapeutic potential of tumor suppressive miR-138 through direct downregulation of CD44 for the treatment of primary GBM.

| S-EPMC8080729 | biostudies-literature

MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

Project description:100 ng of total RNA was processed with the Human v3 miRNA Expression Assay using NanoString nCounter system (NanoString, USA). Expression of individual miRNA was measured by quantitative real-time PCR with TaqMan miRNA Expression kit (Applied Biosystems, Thermo Fisher Scientific, USA).

2021-03-01 | GSE165937 | GEO

Identification of the downstream target genes of miR-138 in gastric cancer

Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.

2021-10-08 | GSE183654 | GEO

Quantitative Proteomics implicates CD44 in proliferation of breast cancer cell

Project description:CD44 is a transmembrane glycoprotein playing a key role in cel adhesion to the extracellular matrix. CD44 expression is upregulated in various cancer cells and recognized as a molecular marker for tumor-initiating cancer cells. However, the intricate correlation between CD44 and underlying biological functions is yet to be fully disclosed at molecular levels. Here, we discovererd global proteome changes induced by CD44 knockdown in the four different breast cancer cell lines by TMT based quantitative proteomics.

2021-06-10 | PXD015171 | Pride

MicroRNA-138 Increases Chemo-Sensitivity of Glioblastoma through Downregulation of Survivin.

Project description:Glioblastoma (GBM) is one of the most deadly cancers and poorly responses to chemotherapies, such as temozolomide (TMZ). Dysregulation of intrinsic signaling pathways in cancer cells are often resulted by dysregulated tumor suppressive microRNAs (miRNAs). Previously, we found miR-138 as one of tumor suppressive miRNAs that were significantly down-regulated in GBM. In this study, we demonstrated that ectopic over-expression of miR-138 sensitizes GBM cells to the treatment of TMZ and increased apoptotic cell death. Mechanistically, miR-138 directly repressed the expression of Survivin, an anti-apoptotic protein, to enhance caspase-induced apoptosis upon TMZ treatment. Using an intracranial GBM xenograft mice model, we also showed that combination of miR-138 with TMZ increases survival rates of the mice compared to the control mice treated with TMZ alone. This study provides strong preclinical evidence of the therapeutic benefit from restoration of miR-138 to sensitize the GBM tumor to conventional chemotherapy.

| S-EPMC8301402 | biostudies-literature

Downregulation of Transmembrane protein 40 by miR-138-5p Suppresses Cell Proliferation and Mobility in Clear Cell Renal Cell Carcinoma.

Project description:Background:Clear cell renal cell carcinoma (ccRCC) represents approximately 70% of RCC,as the most frequent histological subtype of RCC. MiR-138-5p, a tumor-related microRNA (miRNA), has been reported to be implicated in the diverse types of human malignancies, but its role in ccRCCremains unclear. Objective:The study was designed to investigate the functional behaviors and regulatory mechanisms of miR-138-5p in ccRCC. Materials and Methods:Quantitative real-time PCR and western blotting analyses were performed to determine the expression of miR-138-5p and TMEM40 in ccRCC tissues. Pearson's correlation coefficient was utilized to evaluate the correlation between miR-138-5p and TMEM40 expression. The function of miR-138-5p and TMEM40 in the cell proliferation, migration and invasion of ccRCC cells (786-O and ACHN) was assessed by CCK-8, colony formation, wound healing and transwell assay, respectively. A luciferase reporter assay was performed to confirm the direct binding of miR-138-5p to the target gene TMEM40. Results:We found the expression of miR-138-5p was significantly down-regulated, while TMEM40 was remarkably up-regulated in ccRCC tissues. TMEM40 expression was discovered to be inversely correlated with miR-138-5p expression in ccRCC tissues. Functional studies demonstrated that miR-138-5p overexpression or TMEM40 knockdown significantly suppressed ccRCC cell proliferation, migration and invasion in vitro. Notably, we experimentally confirmed that miR-138-5p directly recognizes the 3'-UTR of the TMEM40 transcript and down-regulated its expression in ccRCC cells. Conclusions:Taken together, our findings provide the first clues regarding the role of miR-138-5p as a tumor suppressor in ccRCC by directly targeting of TMEM40.

| S-EPMC7461706 | biostudies-literature

CD44 connects autophagy decline and aging in the vascular endothelium

Project description:The decline of endothelial autophagy is closely related to vascular senescence and disease, although the molecular mechanisms connecting these outcomes in vascular endothelial cells (VECs) remain unclear. Here, we identify a crucial role for CD44, a multifunctional adhesion molecule, in controlling autophagy and aging in VECs. The CD44 intercellular domain (CD44ICD) negatively regulates autophagy by reducing PIK3R4 and PIK3C3 levels and disrupting STAT3-dependent PtdIns3K complexes. CD44 and its homologue clec-31 are increased in aging vascular endothelium and Caenorhabditis elegans, respectively, suggesting that an age-dependent increase in CD44 induces autophagy decline and aging phenotypes. Accordingly, CD44 knockdown ameliorates age-associated phenotypes in VECs. The endothelium-specific CD44ICD knock-in mouse is shorter-lived, with VECs exhibiting obvious premature aging characteristics associated with decreased basal autophagy. Autophagy activation suppresses the premature aging of human and mouse VECs overexpressing CD44ICD, function conserved in the CD44 homologue clec-31 in C. elegans. Our work describes a mechanism coordinated by CD44 function bridging autophagy decline and aging.

2023-08-30 | GSE236523 | GEO

Evaluation of gene expression between CD44+ and CD44- cells in colonospheres

Project description:To identify genes that are differentially expressed between CD44+ and CD44- cells in colonospheres, we have employed whole genome microarray expression profiling as a discovery platform. Colonospheres from four colon cancer patients were sorted into CD44+ and CD44- cells using the FACS Aria II Cell Sorter, and total RNA extracted from the cells were labeled with Cy3 and used for microarray analyses with Agilent Whole Human Genome Oligo Microarrays. Gene expression in fluorescence-activated cell-sorted CD44+ and CD44- cells derived from four colon cancer patients was measured.

2012-12-07 | E-GEOD-38706 | biostudies-arrayexpress

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