Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analyses of prometastasic gene profile and immune infiltration in K7M2 osteosarcoma mouse model after treatment with SFV vectors expressing galectin-3 inhibitor.

ABSTRACT: RNA profiling of orthotopic K7M2 osteosarcoma mouse model treated with SFV-Gal3-N-C12, SFV-Luc or PBS (mock group). To better understand the mechanism underlying the therapeutic effect of SFV-Gal3-N-C12 we analyzed, in primary tumors of treated mices, the changes in expression of osteosarcoma-specific prometastasic genes as well as immunomodulatory molecules genes, and differences in immune cell infiltration.

ORGANISM(S): Mus musculus

PROVIDER: GSE197902 | GEO | 2022/08/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Analyses of prometastasic gene profile and immune infiltration in K7M2 osteosarcoma mouse model after treatment with SFV vectors expressing galectin-3 inhibitor.

Project description:Analyses of prometastasic gene profile and immune infiltration in K7M2 osteosarcoma mouse model after treatment with SFV vectors expressing galectin-3 inhibitor.

| PRJNA812779 | ENA

RNA sequencing of murine osteosarcoma tumors

Project description:We utilized murine osteosarcoma cell lines F420 and K7M2. F420 was originally derived from a female C57BL/6 mouse transgenic for a mutant p53 under control of a bone-selective promoter (PMID: 25579177). K7M2 was derived from a spontaneous metastatic lesion in a female Balb/C background (PMID: 16837208). F420 osteosarcoma tumors were established by subcutaneously injecting 5 x 10^6 osteosarcoma cells into the flanks of 6-week-old C57BL/6 mice (Envigo, Frederick, MD). K7M2 tumors were established by transplanting small pieces of sectioned tumor (~2mm3) into the flanks of 6-week-old Balb/C mice (Envigo). We found K7M2 to be more immunogenic than F420 as it demonstrated higher immune cell infiltrates, higher expression of immune-related genes, and slower growth in syngeneic versus nude models.

2021-06-29 | GSE166282 | GEO

Effect of K7M2 derived extracellular vesicles on gene expression of primary bone marrow derived macrophage

Project description:To profile the molecular changes that are caused by osteosarcoma cell-derived EVs macrophages, we performed RNA-seq of BMDMs treated with K7M2-EVs or the PBS control.

2023-12-31 | GSE205440 | GEO

Genome-wide CRISPR-Cas9 screen to identify SFV4 receptor

Project description:The goal of this study is to identify entry receptor for Semliki Forest virus (SFV, strain SFV4). For this, we used the human genome-wide Brunello CRISPR/Cas9 knockout library in a screen on human osteosarcoma cells (HOS, ATCC, CRL-1543) infected with fully replicative SFV4. While these cells are not a natural target for neurotropic SFV, they offer a highly SFV-permissive and easy to culture model needed for the screen. We performed the screening both with and without the janus kinase (JAK) inhibitor ruxolitinib as we hypothesized that ruxolitinib would limit the host cells capability to resist SFV replication and therefore sensitize the screen more towards factors associated with viral entry

2024-12-12 | GSE283607 | GEO

Molecular changes in the lung during otseosarcoma pre-metastatic niche formation

Project description:To profile the molecular changes in the lung during osteosarcoma pre-metastatic niche formation, we performed RNA-seq of lungs harvested from D0 and D14 after orthotopic implantation of K7M2 cells in balb/c mice.

2024-01-15 | GSE241824 | GEO

LC-MS/MS of extracellular vesicles from murine osteosarcoma cell line K7 and K7M2

Project description:Extracellular vesicles have been shown to be highly enriched in proteins with various functions, including organotropic metastasis. To identify possible protein cargos involved in regulating mestastatic potential of osteosarcoma cell line, we performed quantitative mass spectrometry analysis of EVs from highly metastatic K7M2 cells and poorly metastatic parental K7 cells.

2024-01-15 | PXD035216 | Pride

Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

Project description:Spinal cord injury (SCI) is a debilitating condition within the nervous system with a high disability rate and substantial economic burden. The functional recovery following SCI is enhanced by moderate levels of autophagy but hindered when autophagy becomes excessive. Galectin-3 (GAL3) has been recognized as an autophagy regulator; however, its role in SCI and its associated mechanism are largely unknown. Here we report that GAL3 was increased in spinal neurons and serum in SCI rats, and knockdown or inhibition of GAL3 promoted motor function recovery. The bioinformatics analysis showed that GAL3 is closely related to programmed cell death after SCI. Indeed, the knockdown of GAL3 resulted in a decrease in autophagy markers ATG7 and LC3 II/I ratio, along with an increase in P62 expression. Furthermore, GAL3 and cell division cycle 42 (CDC42) exhibited close associations with neuronal autophagy. Injection of CDC42 inhibitor ML141 effectively reduced GAL3-mediated enhancement of neuronal autophagy. Additionally, CDC42 was increased in spinal neurons post-SCI, and administration of ML141 decreased the expression of autophagy markers and improved motor function recovery. Importantly, elevated levels of GAL3 and CDC42 were observed in the serum of SCI patients. These findings suggest a potential interplay between GAL3 and CDC42 in regulating neuronal autophagy after SCI and indicate the therapeutic potential of targeting this pathway for enhancing recovery from spinal cord injuries.

2024-09-01 | GSE274319 | GEO

Dysregulation of c-terminal ezrin phosphorylation prevents tumor progression and metastasis and alters cellular metabolism in osteosarcoma

Project description:This dataset contains Affymetrix Mouse Genome 430 2.0 Array data obtained from K7M2 cells over-expressing ezrinT567A and the wild-type Gene expression analysis of K7M2 cells over-expressing ezrinT567A compared to the wild-type

2012-03-14 | E-GEOD-33897 | biostudies-arrayexpress

Cancer EVP Uptake in Lung Interstitial Macrophages Enhances Vascular Permeability and Metastatic Potential (in vivo)

Project description:Enhanced vascular permeability in the pre-metastatic niche facilitates tumor cell extravasation and metastasis. Extracellular vesicles and particles (EVPs) are pivotal mediators of cancer progression, including induction of vascular permeability. We identify a novel mechanism whereby melanoma and osteosarcoma EVPs (B16F10 and K7M2) enhance endothelial cell permeability, tumor extravasation and lung metastasis.In contrast, EVPs from breast tumors (4T1 and 67NR) elicited only mild vascular permeability, tumor cell extravasation, and metastasis. EVP induced vascular leakiness is observed within 48h following tumor implantation and as early one hour following direct injection of the B16F10 or K7M2 derived EVPs in non-tumor bearing mice. Rather than acting directly on endothelial cells, EVPs activated interstitial macrophages (IMs) anddepletion of IM with a CSF1R antibody significantly reduced vascular leakiness and metastatic potential.Subsequent activation of JAK/STAT signaling in IMs induces IL-6 secretion which in turn induces endothelial permeability.B16F10 and K7M2 EVPs highly expressed ITGα5 compared to breast tumors, and knock down ofintegrin-α5impairs IM signaling, vascular permeability and metastasis. Furthermore, in patients Il-6 expression is elevated in tumor-adjacent IMs compared to distant tissues. Our findings identify a key role for IMs in mediating tumor type-specific EVP-driven vascular permeability and metastasis, offering promising targets for therapeutic intervention.

2024-06-26 | GSE261138 | GEO

Cancer EVP Uptake in Lung Interstitial Macrophages Enhances Vascular Permeability and Metastatic Potential (in vitro)

Project description:Enhanced vascular permeability in the pre-metastatic niche facilitates tumor cell extravasation and metastasis. Extracellular vesicles and particles (EVPs) are pivotal mediators of cancer progression, including induction of vascular permeability. We identify a novel mechanism whereby melanoma and osteosarcoma EVPs (B16F10 and K7M2) enhance endothelial cell permeability, tumor extravasation and lung metastasis.In contrast, EVPs from breast tumors (4T1 and 67NR) elicited only mild vascular permeability, tumor cell extravasation, and metastasis. EVP induced vascular leakiness is observed within 48h following tumor implantation and as early one hour following direct injection of the B16F10 or K7M2 derived EVPs in non-tumor bearing mice. Rather than acting directly on endothelial cells, EVPs activated interstitial macrophages (IMs) anddepletion of IM with a CSF1R antibody significantly reduced vascular leakiness and metastatic potential.Subsequent activation of JAK/STAT signaling in IMs induces IL-6 secretion which in turn induces endothelial permeability.B16F10 and K7M2 EVPs highly expressed integrin-α5 compared to breast tumors, and knock down ofITGα5impairs IM signaling, vascular permeability and metastasis. Furthermore, in patients Il-6 expression is elevated in tumor-adjacent IMs compared to distant tissues. Our findings identify a key role for IMs in mediating tumor type-specific EVP-driven vascular permeability and metastasis, offering promising targets for therapeutic intervention.

2024-06-26 | GSE261137 | 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