Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Navel Orange Peel Essential Oil Inhibits the Growth and Progression of Triple Negative Breast Cancer

ABSTRACT: Triple Negative Breast Cancer (TNBC) is a particular type of breast cancer with the highest mortality rate and there has been growing concern about the development of essential oils as potential anti-cancer drugs.This investigation explored the bioactivity and molecular mechanisms of navel orange peel oil (NOPEO) against TNBC cells. By initiating cell cycle block and apoptosis, NOPEO demonstrated potent growth suppressive properties on the TNBC cell lines MDA-MB-231 and MDA-MB-453. NOPEO was also effective in inhibiting the motility of MDA-MB-231 cells and in down-regulating the levels of MMP-9 and MMP-2 proteins. Additionally, NOPEO's inhibitory effects on MDA-MB-231 gene expression were analysed by RNA sequencing. In total, 1376 genes were found to be upregulated and 1335 genes were downregulated after NOPEO treatment. According to KEGG and GO pathways, the differentially expressed genes were related to MAPK, Jak/stat and FoxQ signalling pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE253079 | GEO | 2024/06/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Protein Kinase D drives the secretion of invasion mediators in triple negative breast cancer cell lines

Project description:Protein kinase D (PKD) regulates protein secretion at the Golgi complex and has been found to have a pro-oncogenic role in triple-negative breast cancer (TNBC). PKD was previously reported to regulate the secretion of tumor-promoting factors in prostate and pancreatic cancer. Whether PKD plays a similar role in TNBC remains unknown. Here, we used mass spectrometry-based proteomics to characterize the secreted proteome collected from the TNBC cell lines MDA-MB-231 and MDA-MB-468 following pharmacological PKD2 and PKD3 inhibition. Analysis of secretome signatures of response revealed several extracellular matrix related proteins decreased upon PKD inhibition. Amongst the downregulated proteins were previously described TNBC invasion mediators, such as TNC, STC-1, LIF, MMP-1 and M-CSF. The secretion of these proteins, as well as of MMP-13, IL-11 and GM-CSF, was further validated by multiplex assays to be regulated by PKD. Secretion regulation of this protein set by PKD was more evident in TNBC metastatic cell lines than in primary tumor-derived. Individual knockdown of PKD2 and PKD3 revealed that secretion of this protein set is predominantly PKD2-driven in MDA-MB-231 cells. This study improves the current understanding of PKD’s contribution to TNBC secretion and uncovers a novel function of PKD2 in the release of a pro-invasive secretome. / This study improves the current understanding of PKD’s contribution to TNBC secretion and uncovers the distinct pro-invasive substrates of PKD2 and PKD3.

2024-01-17 | PXD041042 | Pride

Metabolic and lipidomic characterization of radioresistant MDA-MB-231 human breast cancer cells to investigate potential therapeutic targets

Project description:To provide preliminary insights into metabolic and lipidomic characteristics in radioresistant triple-negative breast cancer (TNBC) cells and suggest potential therapeutic targets, we performed a comprehensive metabolic and lipidomic profiling of radioresistant MDA-MB-231 (MDA-MB-231/RR) TNBC cells and their parental cells using gas chromatography-mass spectrometry and nano electrospray ionization-mass spectrometry, followed by multivariate statistical analysis. Buthionine sulfoximine (BSO) and radiation were co-treated to radioresistant TNBC cells. The level of glutathione (GSH) was significantly increased, and the levels of GSH synthesis-related metabolites, such as cysteine, glycine, and glutamine were also increased in MDA-MB-231/RR cells. In contrast, the level of lactic acid was significantly reduced. In addition, reactive oxygen species (ROS) level was decreased in MDA-MB-231/RR cells. In the lipidomic profiles of MDA-MB-231/RR cells, the levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were significantly increased, whereas those of most of the phosphatidylinositol species were significantly decreased. BSO sensitized MDA-MB-231/RR cells to radiotherapy, which resulted in decreased GSH level and increased ROS level and apoptosis. Radioresistant TNBC cells showed distinct metabolic and lipidomic characteristics compared to their parental cells. We suggested activated GSH, PC, and PE biosynthesis pathways as potential targets for treating radioresistant TNBC cells. Particularly, enhanced radiosensitivity was achieved by inhibition of GSH biosynthesis in MDA-MB-231/RR cells.

2021-09-22 | ST001920 | MetabolomicsWorkbench

Human Adipocytes Regulate Gene Expression in Triple-negative Breast Cancer Assessed by NGS Sequencing

Project description:Adipocyte was found play a pivotal role in tumorgenesis, progression and metastasis in breast cancer. However, affection of adipocyte on gene expression profile in triple-negative breast cancer (TNBC) is still not clear. In the present study, firstly we reported the gene expression profiles of TNBC regulated by human adipocytes using NGS. TNBC cell MDA-MB-231 was used in this study. MDA-MB-231 cells were treated with medium derived from adipocytes culture supernatants. Using two different RNA libraries, we sequenced the complete transcriptome(including mRNA, lncRNA, circleRNA and small RNA) of MDA-MB-231 treated with medium derived from adipocytes culture supernatants.

2018-09-04 | GSE119377 | GEO

Role of SIPA1 in chemotherapy resistance in breast cancer cells

Project description:SIPA1 is a potential transcriptional modulator of tumor metastasis and recurrence. Here we showed that the breast cancer patients with higher SIPA1 expression have a higher relapse rate and worse prognosis, especially for triple-negative breast cancer (TNBC) patients. Moreover, SIPA1 expression was found positively correlated with relapse of breast cancer patients receiving adjuvant chemotherapy. In a TNBC cell line MDA-MB-231, we identified the possible tumorigenesis and metastasis processes regulated by SIPA1, and demonstrated that SIPA1 promoted cancer stem-like feature to form tumourspheres. Tumoursphere-formed MDA-MB-231 cells were shown to be resistant to epirubicin. Then we confirmed that SIPA1 could particularly activate the CD44 promoter and upregulate CD44 expression. Furthermore, SIPA1 could promote ABCB1 expression and strengthen chemoresistance of MDA-MB-231 cells to epirubicin. In conclusion, SIPA1 is a risk factor for highly-relapse in TNBC patients and a transcriptional regulator to maintain cancer stem-like features and promote chemoresistance in breast cancer cells.

2018-12-25 | GSE124344 | GEO

Effect of silencing of p53 on gene expression in MDA-MB 231 TNBC cell line. [sip53]

Project description:Mutant p53 can acquires oncogenic properties supporting tumor growth, metastases and chemoresistance, by reprogramming cancer cell transcriptome, proteome and metabolome. To investigate what is the gene expression network regulated by mutant p53, we silenced its expression in MDA-MB-231 Triple Negative Breast Cancer (TNBC) cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB 231.

2023-10-06 | GSE214493 | GEO

Gene expression profile in breast cancer cell lines using RNA sequencing

Project description:In order to identify novel molecular targets associated with TNBC progression, we initially performed transcriptome analysis using RNA sequencing in breast cancer cell lines, classified as either the luminal subtype (MCF-7, T47D, ZR-75B) or basal-like subtype (MDA-MB-231, MDA-MB-435, Hs578T).

2017-08-09 | GSE100878 | GEO

LncRNA Uc003xsl.1 Activates of NF-κB/IL8 Axis to Promotes Triple-negative Breast Cancer Progression via A Decoy Role to NKRF [lnc231]

Project description:To discover the potential drivers of TNBC metastasis, we established an in vivo model by injecting MDA-MB-231cells into the tail veins of mice. Then, the breast tumor cells that successfully grew into metastatic lung tumors were collected and expanded in vitro, followed by re-injected into the tail veins of mice for lung metastasis. After three rounds of selection, a highly metastatic subline, MDA-MB-231-P3, was established, and more frequent micro-metastasis was detected in MDA-MB-231-P3 groups than that of MDA-MB-231 groups when the lungs of mice were stained with hematoxylin and eosin (HE). The lncRNA profiles of MDA-MB-231 or MDA-MB-231-P3 cells were analyzed by lncRNA sequencing. A total of 267 lncRNAs in MDA-MB-231-P3 cells were upregulated more than 2-fold in comparison to the MDA-MB-231 cells.

2021-11-29 | GSE163900 | GEO

Inhibitory effect of VNLG-152R on breast cancer cells MDA-MB-231

Project description:In previous studies, our research demonstrated that VNLG-152R exhibits inhibitory effects on Triple Negative Breast Cancer (TNBC) cells both in vitro and in vivo. The TNBC cell line MDA-MB-231 cells were treated with VNLG-152R. A total of 337 genes were differentially expressed when MDA-MB-231 cells were treated with 10 μM VNLG-152R for 24h; 259 genes were upregulated and 78 downregulated. Through proteome analyses, we discovered that VNLG-152R upregulates the expression of E3 ligase Synoviolin 1 (SYVN1), also called 3-hydroxy-3-methylglutaryl reductase degradation (HRD1) in TNBC cells. Moreover, we provide genetic and pharmacological evidence to demonstrate that SYVN1 mediates the ubiquitination and subsequent proteasomal degradation of MNK1/2, the only known kinases responsible for phosphorylating eIF4E. Phosphorylation of eIF4E being a rate-limiting step in the formation of the eIF4F translation initiation complex, the degradation of MNK1/2 by VNLG-152R and its analogs impedes dysregulated translation in TNBC cells, resulting in the inhibition of tumor growth. Importantly, our findings were validated in vivo using TNBC xenograft models derived from MDA-MB-231, MDA-MB-468, and MDA-MB-453 cell lines, representing different racial origins and genetic backgrounds. These xenograft models, which encompass TNBCs with varying androgen receptor (AR) expression levels, were effectively inhibited by oral administration of VNLG-152R and its deuterated analogs in NRG mice.

2023-09-08 | GSE242514 | GEO

human breast cancer cell line LC-MS/MS

Project description:Triple-negative breast cancer (TNBC) is the most aggressive type with poor prognosis among the breast cancers and has a high population of cancer stem cells (CSCs) which are main target to cure and inhibit TNBC. In this study, we analyzed the CSC-related proteome alteration by NEDD4 knockdown in CSC-abundant MDA-MB-231 cells by LC-MS/MS analysis.

2021-09-09 | PXD020585 | Pride

Tang2019 - Pharmacology modelling of AURKB and ZAK interaction in TNBC

Project description:Aurora Kinase B and ZAK interaction model Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018. The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.

2024-09-02 | BIOMD0000000940 | BioModels

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