Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BGN promotes epithelial migration in mammary gland development and breast cancer metastasis through activation of WNT signaling

ABSTRACT: This study investigates the role of Biglycan (BGN) in promoting epithelial migration during mammary gland development and breast cancer metastasis. Using in vitro and in vivo models, including a 3D organoid migration assay and single-cell RNA sequencing, we demonstrate that BGN enhances the interaction between WNT3A and FZD6, activating the WNT signaling pathway. This activation promotes epithelial cell migration and breast cancer metastasis. The findings provide new insights into breast cancer metastasis mechanisms and identify BGN as a potential therapeutic target.

ORGANISM(S): Mus musculus

PROVIDER: GSE279436 | GEO | 2024/10/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BGN promotes epithelial migration in mammary gland development and breast cancer metastasis through activation of WNT signaling

Project description:BGN promotes epithelial migration in mammary gland development and breast cancer metastasis through activation of WNT signaling

| PRJNA1172711 | ENA

Study on the mechanism of BGN in progression and metastasis of ccRCC

Project description:Based on multiple public databases, we investigated the expression level of BGN in ccRCC, its clinical significance, and its association with immune cells. Real-time fluorescence quantitative PCR was employed to validate BGN expression in tumor and adjacent normal tissues. Differential gene analysis, GO-KEGG analysis, and GSEA analysis were performed by RNA sequencing to elucidate the underlying signaling pathways. BGN knockdown cells were generated through lentiviral transfection to examine the impact of BGN on ccRCC. Cell proliferation, migration, and invasion were assessed using CCK8, colony formation, wound healing, Transwell migration, and invasion assays, respectively. Results: Our findings from database analysis and polymerase chain reaction (PCR) revealed a significant upregulation of BGN expression in kidney cancer tissues compared to normal tissues. Further analysis demonstrated a correlation between high BGN expression and ccRCC progression and immune infiltration. In vitro experiments confirmed that BGN silencing effectively inhibited cell proliferation, migration, and invasion of ccRCC. Mechanistically, these effects may be mediated through the MAPK signaling pathway. Conclusion: BGN potentially plays a pivotal role in the progression and metastasis of ccRCC, possibly acting through the MAPK signaling pathway. Therefore, BGN holds promise as a potential therapeutic target for ccRCC.

2024-09-01 | GSE264075 | GEO

Pilot Study 13C flux effects when RhoC or RhoA perturbed (13C BCs)

Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.

2015-02-11 | ST000282 | MetabolomicsWorkbench

Biglycan regulates bone development and regeneration

Project description:Endochondral bone development and regeneration relies on activation and proliferation of periosteum derived-cells (PDCs). Biglycan (Bgn), a small proteoglycan found in extracellular matrix , is known to be expressed in bone and cartilage, however little is known about its influence during bone development. Here we link Bgn with osteoblast maturation starting during embryonic development that with aging affects bone integrity and strength. Bgn gene deletion reduced the inflammatory response after fracture, leading to impaired periostal expansion and callus formation. Using novel 3D scaffold and analyzing newborn bones, we found that Bgn is required for the cartilage-bone transition of PDCs during endochondral bone development. The absence of Bgn led to accelerated bone development with high levels of osteopontin which appeared to be detrimental to the structural integrity of the bone. Collectively, our study identifies Bgn as an important factor in PDCs activation during bone development and bone regeneration after fracture.

2023-03-01 | GSE192542 | GEO

A kinome-wide high-content siRNA screen identifies MEK5-ERK5 signaling as critical for breast cancer cell EMT and metastasis

Project description:We have employed a high-content microscopy screen in combination with a kinome and phosphatome-wide siRNA library to identify signaling pathways underlying an EMT of murine mammary epithelial cells and breast cancer cells. This screen identified the MEK5-ERK5 axis as a critical player in TGFb-mediated EMT. Suppression of MEK5-ERK5 signaling completely prevented the morphological and molecular changes occurring during a TGFb-induced EMT and, conversely, forced highly metastatic breast cancer cells into a differentiated epithelial state. Inhibition of MEK5-ERK5 signaling also repressed breast cancer cell migration and invasion and substantially reduced lung metastasis without affecting primary tumor growth. The results suggest that the MEK5-ERK5 signaling axis plays an important role in the induction and maintenance of breast cancer cell migration and invasion and thus represents an exploitable target for the pharmacological inhibition of cancer cell metastasis.

2018-05-17 | GSE100403 | GEO

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Project description:BRMS1L (breast cancer metastasis suppressor 1 likeM-oM-<M-^LBRMS1-like) is a component of the SIN3A-HDAC corepressor complex that suppresses target gene transcription. Here, we show that reduced BRMS1L in breast cancer tissues is associated with tumor metastasis and poor patient survival. Functionally, BRMS1L inhibits migration and invasion of breast cancer cells by inhibiting epithelial-mesenchymal transition (EMT). These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signaling, by facilitating the recruitment of HDAC1 to its promoter and enhancing histone H3K9 deacetylation. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10-M-oM-^AM-"-catenin signaling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNAi-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, while ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signaling in breast cancer cells and acts as a breast cancer metastasis suppressor. Ther transfection analysis used here were further desxribed in Chang Gong, eta al.2013. miR-106b expression determines the proliferation paradox of TGF-M-NM-2 in breast cancer cells. Oncogene. 2013 A two chip study using total RNA recovered from MDA-MB-231 breast cancer cells transfected with negative control vector or vector overexpressing BRMS1L for 24 hours. Each chip measures the expression 45033 genes were collected from the authoritative data source including NCBI.

2014-09-12 | E-GEOD-61354 | biostudies-arrayexpress

ANILLIN REGULATES BREAST CANCER CELL MIGRATION, GROWTH AND METASTASIS BY NON-CANONICAL MECHANISMS INVOLVING CONTROL OF CELL STEMNESS AND DIFFERENTIATION

Project description:Breast cancer metastasis is driven by profound remodeling of the intracellular cytoskeleton enabling efficient cell migration. Anillin is a unique cytoskeletal scaffolding protein that regulates actin filaments, microtubules, septin polymers and Rho GTPases. Anillin is markedly overexpressed in breast cancer and other solid cancer, however its functions in cancer cells remain poorly understood. This study aims at investigating the roles of anillin in regulating breast cancer cell migration, invasion and metastasis. CRISPR/Cas9 technology was used to deplete anillin in highly metastatic MDA-MB-231and BT549 cells and to overexpress it in poorly invasive MCF10AneoT cells. These loss-of-function and gain-of-function studies demonstrated that anillin is necessary and sufficient to accelerate migration, invasion and anchorage-independent growth of breast cancer cells in vitro. Furthermore, loss of anillin markedly attenuated both primary tumor growth and metastasis of breast cancer in vivo. In breast cancer cells, anillin was localized in the nucleus, however anillin knockout affected the cytoplasmic/cortical events such as the organization of actin cytoskeleton and cell-matrix adhesions. This was accompanied by a global transcriptional reprogramming of anillin-depleted breast cancer cells that resulted in suppression of their stemness and induction of the mesenchymal to epithelial trans-differentiation. Such trans-differentiation was manifested by upregulation of basal keratins along with increased expression of E-cadherin and P-cadherin. Knockdown of E-cadherin reversed attenuated migration and invasion of anillin-deficient cells. Our study provides the first evidence that anillin plays causal roles in breast cancer development and metastasis in vitro and in vivo and unravels novel functions of anillin in regulating breast cancer stemness and differentiation.

2020-01-01 | GSE131120 | GEO

Transcriptome of EMT induced MCF10A cells by TGFb treatment or SNAIL S6A expression.

Project description:EMT, Epithelial to mesenchymal transition is a developmental biology process associated with migration, known to be involved in cancer metastasis. To study this process, we used the breast epithelial cell line MCF10A that enter in EMT after treatment with the cytokine TGFB or by expression of EMT transcriptor factor SNAIL.

2017-01-30 | GSE89152 | GEO

LncRNA and mRNA expression data from Control or IL-8 overexpressed MCF7 cells

Project description:Metastasis is one of the pivotal causes of high breast cancer mortality, which is consist of epithelial-to-mesenchymal transition (EMT), migration, invasion. While long noncoding RNAs (lncRNAs) are implicated in a variety of diseases, their role in breast cancer is not well understood. IL-8 has been reported to induce EMT of breast cancer cell. In this study, we used microarrays to identify dysregulated lncRNAs and mRNAs underlying IL-8-induced EMT.

2023-08-21 | GSE201574 | GEO

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Project description:BRMS1L (breast cancer metastasis suppressor 1 like，BRMS1-like) is a component of the SIN3A-HDAC corepressor complex that suppresses target gene transcription. Here, we show that reduced BRMS1L in breast cancer tissues is associated with tumor metastasis and poor patient survival. Functionally, BRMS1L inhibits migration and invasion of breast cancer cells by inhibiting epithelial-mesenchymal transition (EMT). These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signaling, by facilitating the recruitment of HDAC1 to its promoter and enhancing histone H3K9 deacetylation. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10--catenin signaling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNAi-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, while ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signaling in breast cancer cells and acts as a breast cancer metastasis suppressor. Ther transfection analysis used here were further desxribed in Chang Gong, eta al.2013. miR-106b expression determines the proliferation paradox of TGF-β in breast cancer cells. Oncogene. 2013

2014-09-12 | GSE61354 | 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