Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Catestatin impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways

ABSTRACT: Melanoma remains one of the most aggressive and treatment-resistant cancers, emphasizing the need for novel therapeutics. In our current study we report a peptide-based approach as potential therapeutic. The expression and role of Catestatin(CST), a Chromogranin A(CgA)-derived peptide with immunomodulatory and reparative properties in skin injury led us to examine its connection to melanoma. Advancing melanoma stages showed decreased CST expression. CST administration to patient derived cells and melanoma cell lines A375, B16F10, SKMEL28 revealed increased apoptosis, decreased proliferation and metastatic ability of the melanoma cells without affecting cell viability for normal skin fibroblasts. CST reduced growth kinetics and tumor weight in B16F10 derived in vivo melanoma tumors. Transcriptomic analyses of catestatin treated human cell line and mouse tumor revealed downregulation of hypoxia, collagen remodeling, epithelial to mesenchymal transition pathways (EMT), stress adaptive responses that are accountable for melanoma progression. In Vemurafenib-resistant A375 cells, CST increased apoptosis and repressed multiple resistance associated genes. These results highlight CST as a promising therapeutic candidate capable of opposing melanoma progression and overcoming resistance to current targeted treatments.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE312638 | GEO | 2026/03/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

New compounds triggering endoplasmic reticulum stress exert anti-melanoma effects and overcome BRAF inhibitor resistance

Project description:We discovered and developed a new series of molecules (thiazole benzenesulfonamides). HA15, the lead compound of this series, displayed anti-cancerous activity on all tested melanoma cells including those isolated from patients and those that developed resistance to BRAF inhibitors. Our molecule displayed activity against other liquid and solid tumors. HA15 also exhibited strong efficacy in xenograft mouse models with melanoma cells either sensitive or resistant to BRAF inhibitors. Transcriptomic, proteomic and biochemical studies identified the chaperone BiP/GRP78/HSPA5 as the specific target of HA15 and demonstrated that the interaction increases endoplasmic reticulum (ER) stress, leading to melanoma cell death by concomitant induction of autophagic and apoptotic mechanisms. Profiling of 3 human melanoma cell lines (SKMel28, Mel501, A375) treated with HA15 at 10 uM or with DMSO was performed using whole genome human microarrays. Cells were incubated with DMSO or HA15 for 6h and then lysed prior to RNA isolation, labelling and hybridization on microarrays. One color experiment, total of 6 samples.

2016-06-01 | E-GEOD-79071 | biostudies-arrayexpress

miR-146a promotes the initiation and progression of melanoma by activating Notch signaling

Project description:Oncogenic mutations in BRAF and NRAS occur in 70% of melanomas. Here we identify a microRNA, miR-146a, that is highly upregulated by oncogenic BRAF and NRAS. Expression of miR-146a increases the ability of human melanoma cells to proliferate in culture and form tumors in mice, whereas knockdown of miR-146a has the opposite effects. We show these oncogenic activities are due to miR-146a targeting the NUMB mRNA, a repressor of Notch signaling. Previous studies have shown that pre-miR-146a contains a single nucleotide polymorphism (C>G rs2910164). We find that the ability of pre-miR-146a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR-146a/C. Analysis of melanoma cell lines and matched patient samples indicates that during melanoma progression pre-miR-146a/G is enriched relative to pre-miR-146a/C, resulting from a C-to-G somatic mutation in pre-miR-146a/C. Collectively, our results reveal a central role for miR-146a in the initiation and progression of melanoma. SKMEL28 melanoma cell line stably expressing either an empty vector or pre-miR146a with either C or G SNP (SKMEL28-FG12, SKMEL28-miR-146a/C and SKMEL28-miR-146a/G) were used to prepare total RNA. Microarray analysis was performed by using biological replicates for each stable cell lines for a total of 6 samples.

2014-02-18 | E-GEOD-39294 | biostudies-arrayexpress

A four-arm study of A375 melanoma cell line-derived xenograft tumors in NSG mice treated with Vemurafenib and CB839

Project description:Melanoma is a rare but deadly form of skin cancer, which is often treated with BRAF inhibitors such as Vemurafenib (referred to as PLX4032). Whilst Vemurafenib prolongs the survival of patients, BRAF inhibitor resistance inevitably occurs in most cases. Previous studies demonstrated that metabolic rewiring occurs in BRAF inhibitor resistance and causes dependence on glutamine. To investigate whether this vulnerability could be exploited with clinically relevant drugs, we used the BRAF inhibitor, Vemurafenib, and the glutaminase imhibitor, CB839 to treat A375-derived melanoma xenografted tumors. We showed that whilst CB839 did not significantly affect the growth of A375-derived tumors compared to those given a vehicle, the addition of CB839 to Vemurafenib treatment had a significant anti-tumor effect. Tumors were taken at the endpoint (Max tumor length 15mm) from the 6 mice in each treatment group and cut into fragments and stored in RNAlater for RNAseq analysis. RNA extraction was performed on 1-3 fragments per tumor to make up 200-300mg of tissue.

2023-04-07 | E-MTAB-12811 | biostudies-arrayexpress

Human melanoma cell lines secretome analysis

Project description:The imbalance of cellular homeostasis during oncogenesis together with the high heterogeneity of tumor-associated stromal cells have a marked effect on the repertoire of the proteins secreted by malignant cells (the secretome). Hence, the study of tumoral secretomes provides insights for understanding the cross-talk between cells within the tumor microenvironment as well as the key effectors for the establishment of the pre-metastatic niche in distant tumor sites. In this context, we performed a proteomic analysis of the secretomes derived from four cell lines: (i) a paired set of fibroblasts - Hs 895. T, a cell line obtained from a lung node metastatic site from a patient who had melanoma and Hs 895.Sk, a skin fibroblast cell line (derived from the same patient); (ii) two malignant metastatic melanoma cell lines - A375, a malignant melanoma cell line from primary source and SH-4, a cell line derived from pleural effusion of a patient with metastatic melanoma. Clustering of expression profiles together with functional enrichment revealed patterns that mirrored each cell type (skin fibroblasts, cancer-associated fibroblasts and metastatic cells). These patterns might be the result of cell-specific protein expression programs and may serve as basis for further proteomic analysis of melanoma cell lines secretomes.

2018-01-02 | PXD007265 | Pride

EXP. 229_AC_RNAseq data of human cancer cell lines 94T778, SKBR3, AU565, SKMEL28 and A375 exposed to the selective MTOR inhibitor torkinib (PP242, Selleckchem, TX, USA) for 72 hours.

Project description:Drug concentrations were selected to halt cell cycle progression without affecting cell viability: 94T778 10 µM, A375, SKMEL28 and AU565 4 µM, SKBR3 0.8 µM. The pharmacologic inhibition of MTOR repressed expression of the homologous recombination (HR) and Fanconi Anemia (FA) pathways, and selectively high-fidelity but not error-prone DNA polymerases in all cancer cell lines sequenced

2020-04-09 | GSE148344 | GEO

RNA transcriptome sequencing of Skin Cutaneous Melanoma cell line A375 and SK-MEL-28 treated with siNC or siLINC01291

Project description:To figure out the role of long non-coding RNA LINC01291 in Skin Cutaneous Melanoma and the underlying mechanism, RNA transcriptome sequencing was performed to globally characterize LINC01291-regulated transcriptome changes. LINC01291 knockdown by siRNA in melanoma cells. A375 and SK-MEL-28 cells treated with siNC served as control.

2025-12-31 | GSE285702 | GEO

Transcription profiling of mouse B16-F10 melanoma cells stimulated with TIM-3

Project description:The effect of TIM-3 stimulation was studied on B16F10 mouse melanoma cells, in vitro. Experiment Overall Design: Cy3: B16F10 mouse melanoma cells, treated by unspecific goat IgG (control) for 2 hours. Experiment Overall Design: Cy5: B16F10 mouse melanoma cells, in vitro, treated by an agonist goat polyclonal anti-mouse TIM3 antibody (RnD Systems) for 2 hours. Experiment Overall Design: Four biological replicates were used (in this study, biological replicate means different passage numbers of the same cell line). In each case, the treated sample (Cy5) was compared to its control one (Cy3) in Agilent dual-color microarray experiments.

2009-10-15 | E-GEOD-14418 | biostudies-arrayexpress

Effect of Omomyc on the in vitro growth of A375 human melanoma cell line

Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in melanoma cells in vitro in A375 (mutated in BRAF) melanoma cell line. We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 4.

2023-04-09 | GSE227840 | GEO

MHC1-TIP: scalable multimodal immunopeptidome profiling of low-input samples

Project description:We developed MHC1-TIP: an optimized mild acid elution-based immunopeptidomics workflow that leverages data independent acquisition and the Astral mass analyzer to enable scalable, single-tube and cost-effective MHC-I ligandome profiling. This dataset includes immunopeptidomics and proteomics data from the A375 melanoma cell line, colorectal cancer patient-derived organoids, and renal cell carcinoma tumour fragments. We show the effects of TGF-beta treatment on the proteome and immunopeptidome of A375 cells and interferon-gamma treatment on patient-derived organoids. We also explore immunopeptidome and proteome heterogeneity in patient-derived tumour fragments. MB_30: A375 immunopeptidomes in DDA (wildtype and B2M knockout); MB_38: Proteomes with and without mild acid treatment with A375 cells; MB_39: Proteomes and immunopeptidomes from TGFb treated A375 cells; MB_41: MHC1-TIP and MHC-I immunoprecipitation data from different A375 cell input numbers; MB_43: immunopeptidomes of A375 cells treated with different doses of interferon-gamma; MB_45: immunopeptidomes of A375 cells with MHC1-TIP and immunoprecipitation after mild acid elution to identify intracellular peptides; MB_46: Proteomics and immunopeptidomics data from 15 ex-vivo cultured patient-derived tumour fragments; MB_49: Proteomics and immunopeptidomics data from 3 patient-derived organoid lines.

2025-12-18 | PXD065279 | Pride

Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

Project description:Melanoma is the most deadly type of skin cancers and, there is a continuous need to develop early biomarkers as well as treatments to improve the survivability of patients. Ambra1 is an essential regulator in autophagy and it has been recently shown to have a role in cell proliferation. We used microarrays to analyse the transcriptomic changesi n A375 melanoma cell lines following Ambra1 differential expression

2021-05-23 | GSE175361 | 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