Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Carnosol alleviating C26 induced Cancer Cachexia

ABSTRACT: Shotgun proteomics using LC-high resolution tandem mass spectrometry was applied to check the protein expression profiles of C2C12 myotubes in control group (treated with solvent control 0.1% DMSO), C26 medium group (treated with conditioned medium of C26 tumor cells for 48 h), CS group (treated with car-nosol at 20 μM for 48 h) and C26+CS group (treated with conditioned medium of C26 tumor cells in the presence of 20 μM carnosol for 48 h). Samples of three independent experiments were collected.

ORGANISM(S): Mus Musculus

SUBMITTER: Xuan Liu

PROVIDER: PXD043464 | iProX | Sun Jul 02 00:00:00 BST 2023

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

Phosphoproteomic analysis of C2C12 myotubes induction of C26 medium, TNF-α and IL-6

Project description:The C2C12 cells (10000 cells/mL) were seeded into 100 mm cell culture dishes and induced to differentiation into myotubes. C2C12 myotubes were treated with simulated cancer cachexia injuries including conditioned medium (CM) of C26 colon adenocarcinoma cells or inflammatory cytokines (IL-6 or TNF-α). Then, cells were obtained by trypsin digestion and centrifugation. Samples from four independent experiments were collected.

2025-03-27 | PXD062287 |

C2C12 murine myoblast cell line and 48 h 10 uM BIO treated C2C12 cellulate

Project description:In urodele amphibians, limb regeneration involves the dedifferentiation of muscle myotubes into single cells that may acquire pluripotent potential. We have employed small molecules (myoseverin and BIO) to attempt to reproduce this behavior in mammalian muscle culture. C2C12 myotubes derived from the C2C12 myoblast cell line were induced to undergo cellularization by myoseverin treatment, which destabilizes tubulin filaments. The GSK-3 inhibitor, BIO, was then used to induce dedifferentiation. Induce neuron formation; the cells were incubated with 250 nM reversine for 48 h, and neural induction media (DMEM/F12 supplemented with N2 (Invitrogen)) and 1.5 uM all-trans retinoic acid for 7 days. C2C12 murine myoblast cell line and 48 h 10 uM BIO treated C2C12 cellulate (derived by 20 M myoseverin treatment for 48 h) C2C12 myoblasts were differentiated into myotubes with 2%horse serum in DMEM for 8 days (from 2-4 d, 10 uM AraC treatment was also used to kill any remaining myoblasts). Next, myotubes were cellularized by 20 uM myoseverin treatment for 48 h. 24 h after myoseverin treatment, myotubes were treated with 10 uM BIO for 2d.

2011-12-08 | E-GEOD-34238 | biostudies-arrayexpress

C2C12 murine myoblast cell line and 48 h 10 uM BIO treated C2C12 cellulate

2011-12-08 | GSE34238 | GEO

RNA sequencing of mouse myotubes C2C12 along with treatment of S2-013 conditioned media with and without resveratrol

Project description:RNA was sequenced from differentiated C2C12 mouse myotubes that were treated with S2-013 conditioned media with or without resveratrol in comparison to control media

2020-05-10 | GSE147554 | GEO

Transcriptome changes during the differentiation of myoblasts into myotubes

Project description:This study aimed to interrogate the interrelationship between 3D genome organization and global gene expression during muscle development using a mouse C2C12 cell line as an in vitro model. The C2C12 cell line is a well-established and extensively studied in vitro model derived from serial passage of myoblasts cultured from the thigh muscle of C3H mice after a crush injury. C2C12 cells divide when mitogens are present in the culture medium and spontaneously differentiate into muscle-like multinucleated (myotubes) cells if the medium is depleted of mitogens (i.e. serum; (Bischoff 1986)). C2C12 cells were either harvested as: 1) proliferating myoblasts (Myoblasts); 2) myotubes that were not treated with AraC (as such these myotubes contained myoblasts) - Myotubes(Day3); or 3) myotubes which were treated with AraC (myoblasts were largely depleted from these myotube cultures; Myotubes(Day7+AraC).

2017-04-07 | GSE84158 | GEO

Conditioned media from Cancer cell lines regulate mRNAs in differentiated human muscle stem cells

Project description:To investigate whether conditioned medium (CM) from cancer cell culture impacts dynamic changes of the transcriptome in myotubes differentiated from hMuSC, we ran RNA sequencing from differentiated hMuSC that were treated by multiple breast cancer cell lines-conditioned medium. Among 14208 readable mRNAs, MCF-7 CM treatment induced significant changes in 2680 genes, MB-468 CM caused significant changes in 2674 genes, and SKBR-3 CM resulted in significant changes in 1823 genes in myotubes from differentiated hMuSC, compared to control group, respectively. Among them, 961 genes had significant upregulation or downregulation presented in differentiated myotubes over all 3 breast cancer cell lines CMs

2023-05-03 | GSE206662 | GEO

Control of FoxO1 mRNA expression by microRNAs

Project description:To identify miRNAs, a microarray analysis were differentially expressed between C2C12 myotubes stimulated with 1 μM clenbuterol for 1 h and their control myotubes.

2019-04-24 | GSE130181 | GEO

Effect of a 24h corticosterone treatment on differentiated C2C12 myotubes

Project description:Long term glucocorticoïds treatment, e.g. corticosterone, induces insulin resistance in vivo and in vitro. In vivo insulin resistance can trigger pancreatic beta cells adaptation in order to maintain glycemia. In particular, we observed that beta-cell mass adaptation can occur via beta-cell proliferation or via beta-cell neogenesis (de novo beta-cell production). Further, we demonstrated that beta-cell neogenesis was not a direct effect of GC, but rather due to the presence of pro-neogenic factors in the serum of GC-treated mice, suggesting a communication in-between insulin resistant tissues and the pancreas (Courty et al., Diabetes, 2019). Hence, the present work aims to decipher the role of the skeletal muscle in pancreatic adaptation in response to insulin resistance. We used an in vitro modeling in-between C2C12 differentiated myotubes treated for 24h with corticosterone (10-7M) or the same volume of solvant ethanol (VEH). Conditioned medium from corticosterone treated cells was tested on pancreatic buds E11.5 and proven to enhance beta-cell and other pro-endocrine lineage cellular differentiation in comparison to VEH conditioned medium. Subsequently, we analyzed the transcriptome of the C2C12 myotubes (n=3 per condition) using RNAsequencing (Illumina, NOVAseq 6000, 150bp paired-end sequencing). We found an enrichement for genes coding for secreted proteins in the CORT-treated myotubes. We narrowed down to 4 myokines candidates and validated the pro-neogenic potential of the candidate myokines using pancreatic buds E11.5 treated with recombinant proteins.

2025-09-10 | GSE261984 | GEO

Genome-wide analysis of gene expression during differentiation in C2C12 cells

Project description:Investigate the genome-wide gene expression profiles of 50% and 95% confluent C2C12 myoblasts and C2C12 myotubes differentiated for 24 and 48 hours.

2010-01-27 | GSE20059 | GEO

Transcriptomic profiling of co-cultured cancer-host cells identifies hypoxia as a driver of the skeletal muscle cell’s antiproliferative effect on cancer cells

Project description:Cancer metastasis is the leading cause of cancer-related death. While organs such as the lung are hotspots for metastases, others -like skeletal muscle- remain rarely colonized, a phenomenon that remains poorly understood. In this study, we show that EO771 breast cancer cells proliferated robustly when co-cultured with MLg lung stromal cells, whereas their proliferation was restrained when maintained in direct contact with differentiated C2C12 skeletal muscle myotubes. Notably, these effects were not cell-typespecific, as similar results were obtained with 4T1 breast cancer cells and Sol8 myotubes. After two days of co-culture, both cancer and host cells (MLg and C2C12) exhibited distinct niche-specific transcriptional remodeling. Strikingly, the poorly proliferative EO771 cells co-cultured with C2C12 myotubes acquired a hypoxia-associated gene-expression signature despite normoxic conditions (~20% O₂), showing that muscle cells reprogram cancer cells into a hypoxic, anti-proliferative state. Under hypoxic conditions, we confirmed that the depletion of oxygen allows C2C12 cells to nearly abolish EO771 proliferation. Neither exogenous lactate, culture acidosis, their combination, altered glucose levels, nor conditioned medium could reproduce the suppressive environment created by C2C12 myotubes. In contrast, MLg cells induced minimal transcriptional changes in EO771 cells and were themselves broadly reprogrammed by the cancer cells. Moreover, hypoxia enhanced EO771 proliferation in MLg co-cultures, emphasizing the permissive nature of the MLg environment. Collectively, these findings uncover a unique, paradoxical, muscleinduced pseudo-hypoxic program that restricts cancer cell proliferation. They also highlight the need for caution in targeting hypoxia signaling in anti-metastatic therapies, as such interventions could weaken skeletal muscle’s natural defense against tumor colonization.

2026-02-06 | GSE299422 | 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