Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of knockdown of GRP94 on gene expression of MKN-45 cells

ABSTRACT: Anoikis resistance allows cancer cells to avoid death caused by detachment from the extracellular matrix's adhesion, enabling these cells to infiltrate and migrate to regions such as the peritoneum.Glucose-regulated protein 94 (GRP94, alternatively labeled as HSP90B1) is typically stress-induced and is part of the heat shock protein 90 (Hsp90) family.GRP94 is closely tied to cellular resistance to stress, apoptosis, proliferation, invasion, inflammation, and immunity.Our findings indicated that while attached culture didn't impact the apoptosis rate between shGRP94 and shCtrl groups, GRP94 knockdown weakened anoikis resistance, migration, and invasion abilities. Here, we aim to assess the impact of knocking down GRP94 on gene expression in the gastric cancer cell line MKN-45, to further elucidate potential molecular mechanisms by which GRP94 affects the biological characteristics of gastric cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267811 | GEO | 2024/07/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps in gastric cancer MKN-45 cells with or without the overexpression of transcriptional factor SIX2

Project description:Analysis of MKN-45 cells following SIX2 stable overexpression or not. SIX2 regulates various mRNA expression in MKN-45 cells.Results provide insight into the role of SIX2-involved mechanisms underlying SIX2-mediated effects on gastric cancer stemness.

2024-06-09 | GSE234584 | GEO

microarray Analysis of MKN-45 cell lines after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.

Project description:We demonstrate that miR-125b, a key node in this microRNA regulatory network, is upregulated in gastric cancer (GC) and associated with poor overall survival through an integrated analysis of microRNA and mRNA profiling of GC revealed a mRNA-regulatory network.So we have employed whole genome microarray expression profiling as a discovery platform to compare the transcriptome profiling of human gastric cells (MKN-45) after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.Pathway analysis shows that the predicted targets of miR-125b are highly involved in apoptosis/program death pathway，and the robust apoptosis genes, BIK and CASP6 are validated as the directed targets of miR-125b.

2021-02-25 | GSE145959 | GEO

Effect of knockdown of GRP94 on gene expression of MKN-45 cells

Project description:Effect of knockdown of GRP94 on gene expression of MKN-45 cells

| PRJNA1113161 | ENA

Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [RNA-seq]

Project description:To investigate the role of Fusobacterium nucleatum (Fn) in the development of gastric cancer, we extracted exosomes from the culture supernatant of MKN-28 cells treated with Fn or PBS, co-cultured them with AGS cells, and analyzed their RNA-seq data for gene expression profiling.

2023-06-07 | GSE214817 | GEO

Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [miRNA-seq]

2023-06-07 | GSE213833 | GEO

Gene expression profiling data following PTBP1 knockout in MKN-28 cells

Project description:We analysed the transcriptome profile by RNA-seq in PTBP1 knockout and control MKN-28 cells.

2021-04-14 | GSE157582 | GEO

Transcriptome analysis of highly metastatic cell line

Project description:A prediction of peritoneal recurrence is of significance using metastasis-related biomarker. This work describes a combined analysis of proteome and transcriptome data for biomarker discovery in highly metastatic cell line. We used nano-flow liquid chromatography (LC) linear ion trap time-of-flight mass spectrometry (LIT-TOF MS) and cDNA microarray to identify specific protein differentially expressed between a highly metastatic stomach cancer cell line MKN-45-P and its parental cell line MKN-45. In total, 240 proteins were found to be expressed between the two cell lines. Of these, 75 proteins (31%) and 49 proteins (20%) were only identified from MKN-45-P and MKN-45 respectively. An mRNA expression of 1533 genes was up-regulated in MKN-45-P compared with MKN-45. No close correlation was found between proteomic and transcriptomic analysis. Interestingly, 4 of 240 proteins (1.6%) were involved in the up-regulated mRNA expression. Comparison analysis of gene expression between highly metastatic gastric cancer cell line MKN-45-P and its parental cell line MKN-45.

2010-06-08 | E-GEOD-21328 | biostudies-arrayexpress

Metastasis-relevant cellular constrictions as determinants for resistance to cell death and cancer aggressiveness

Project description:How mechanical stress might influence the resistance of cancer cells to cell death is currently unknown. To address this, we mimicked the mechanical constrictions that cancer cells might encounter when invading through rich tumoral stroma or undergoing intra- and extravasation. We found that extreme constrictional migration (ECM) but not compression increases the resistance of breast cancer cells to anoikis, a variant of apoptosis triggered by loss of cell adhesions. We also found that Inhibitory of Apoptosis Proteins (IAPs) are responsible for ECM-triggered resistance to anoikis. Together with enhanced cell motility and resistance to natural killer-mediated immune-surveillance, we show that anoikis resistant ECM mechanically-challenged cancer cells have a marked advantage to form lung metastatic lesions. Taken together, our study connects the constrictional mechanical stress typically characterizing the metastatic colonization with the resistance to cell death, while therapeutically targeting the IAPs by SMAC mimetics could counteract anoikis resistance in breast cancer cells.

2022-02-16 | GSE176081 | GEO

GRP94 rewires and buffers the FLT3-ITD signaling network and promotes survival of acute myeloid leukemic stem cells

Project description:Internal tandem duplications in the tyrosine kinase receptor FLT3 (FLT3-ITD) are among the most common lesions in acute myeloid leukemia (AML) and there exists a need for new forms of treatment. Using ex vivo drug sensitivity screening, we found that FLT3-ITD+ patient cells are particularly sensitive to HSP90 inhibitors. While it is well known that HSP90 is important for FLT3-ITD stability, we found that HSP90 family members play a much more complex role in FLT3-ITD signaling than previously appreciated. First, we found that FLT3-ITD activates the unfolded protein response (UPR), leading to increased expression of GRP94/HSP90B1. GRP94 rewires FLT3-ITD signaling by binding and retaining FLT3-ITD in the ER, where it aberrantly activates downstream signaling pathways. Second, HSP90 family proteins protect FLT3-ITD+ AML cells against apoptosis by alleviating proteotoxic stress, and treatment with HSP90 inhibitors results in proteotoxic overload that triggers UPR-induced apoptosis. Importantly, leukemic stem cells are strongly dependent upon HSP90 for their survival, and the HSP90 inhibitor ganetespib causes leukemic stem cell exhaustion in mouse PDX models. Taken together, our study reveals a molecular basis for HSP90 addiction of FLT3-ITD+ AML cells and provides a rationale for including HSP90 inhibitors in the treatment regime for FLT3-ITD+ AML.

2020-09-02 | PXD009423 | Pride

UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three GNE-silencing samples and three control samples.

2010-08-01 | E-GEOD-22336 | 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