Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sensory nerves enhance triple negative breast cancer migration and metastasis through PlexinB3 signaling

ABSTRACT: We identified sensory nerves as more abundant in triple-negative human breast tumors. Human triple negative breast cancer (TNBC) cells (MDA-MB-231, SUM159) were co-cultured with mice primary sensory neurons from dorsal root ganglia (DRG). Breast can-cer cells were found to attach to neurons and have higher migration speed and prolifera-tion rate. Species-specific RNA sequencing highlighted cell migration and adhesion among the most upregulated pathways for cancer cells in coculture. We identified a novel mechanism where cancer’s PlexinB3 interacted with neuron’s Sema5A to regulate attachment and migration along nerve fibers. These findings demonstrate that sensory nerves induced a drastic shift in TNBC cells gene expression, and that dirupting the nerve-cancer is a viable strategy to impede metastasis

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE180508 | GEO | 2021/07/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Sensory nerves enhance triple negative breast cancer migration and metastasis through PlexinB3 signaling

Project description:Sensory nerves enhance triple negative breast cancer migration and metastasis through PlexinB3 signaling

| PRJNA748434 | ENA

Rat motor and sensory nerve LC-MSMS

Project description:Peripheral nerve repair and functional recovery depend on the rate of nerve regeneration and the quality of target reinnervation. It is important to fully understand the cellular and molecular basis underlying the specificity of peripheral nerve regeneration, which means the achieving of respective correct pathfinding and accurate target reinnervation for regrowing motor and sensory axons. In this study, a quantitative proteomic technique, based on isobaric tags for relative and absolute quantitation (iTRAQ) was used to profile the protein expression pattern between single motor and sensory nerves at 14 days after peripheral nerve transection. Among a total of 1259 proteins identified, 176 proteins showed the differential expressions between injured motor and sensory nerves. Quantitative real-time RT-PCR and Western blot analysis were applied to validate the proteomic data on representative differentially expressed proteins. Functional categorization indicated that differentially expressed proteins were linked to a diverse array of molecular functions, including axonogenesis, response to axon injury, tissue remodeling, axon ensheathment, cell proliferation and adhesion, vesicle-mediated transport, response to oxidative stress, internal signal cascade, and macromolecular complex assembly, which might play an essential role in peripheral motor and sensory nerve regeneration. Overall, we hope that the proteomic database obtained in this study could serve as a solid foundation for the comprehensive investigation of differentially expressed proteins between injured motor and sensory nerves and for the mechanism elucidation of the specificity of peripheral nerve regeneration.

2020-12-10 | PXD022097 | Pride

Motor nerves direct the development of the sympathetic nervous system

Project description:The sympathetic nervous system controls a wide spectrum of bodily functions including operation of vessels, cardiac rhythm, and the “flight or fight response”. Sympathetic neurons, which are neural crest-derived, develop in coordination with presynaptic motor nerves extending from the central nervous system (CNS). By using nerve-selective genetic ablations, we revealed that sympathetic ganglia development depends on CNS-derived motor innervation. In the absence of preganglionic motor nerves, trunk sympathetic chain ganglia were fragmented and smaller in size, while cervical ganglia were severely misshapen. Sympathetic neurons were misplaced along sensory fibers and projected towards abnormal paths, in some cases invading the sensory dorsal root ganglia. The misplaced progenitors of sympathoblasts corresponded to the nerve-associated, neural crest-derived Schwann cell precursors (SCPs). Notably, we found that SCPs activate the autonomic marker PHOX2B while migrating along motor nerves towards the region of the dorsal aorta in wildtype embryos, suggesting that SCP differentiate into sympathetic neurons while still nerve-associated in motor-ablated embryos. Ligand-receptor prediction from single cell transcriptomic data coupled with functional studies identified Semaphorin 3A/3F as candidate motor nerve-derived signals influencing neural crest migration along axons. Thus, motor nerves control the placement of sympathoblasts and their subsequent axonal navigation during critical periods of sympathetic chain development.

2024-07-14 | GSE261748 | GEO

FZD7 Plays a Critical Role in Triple Negative Breast Cancer Proliferation

Project description:Breast cancer is genetically and clinically heterogeneous. Triple negative cancer (TNBC) is a subtype of breast cancer usually associated with poor outcome and lack of benefit from target therapy. A pathway analysis in a microarray study was performed using TNBC compared with non-triple negative breast cancer (non-TNBC). Overexpression of several Wnt pathway genes, such as frizzled homolog 7 (FZD7), Low density lipoprotein receptor-related protein 6 (LRP6) and transcription factor 7 (TCF7) has been observed in TNBC. Focus was given to the Wnt pathway receptor, FZD7. To validate its function, inhibition of FZD7 using FZD7shRNA was carried out. Notably decreased cell proliferation, suppressed invasiveness and colony formation in triple negative MDA-MB-231 and BT-20 cells were observed. Mechanism study indicated that these effects occurred through silencing the canonical Wnt signaling pathway, as evidenced by loss of nuclear accumulation of ï?¢-catenin and decreased transcriptional activity of TCF7. In vivo study revealed that FZD7shRNA significantly suppressed the tumor formation in xenotransplation mice due to decrease cell proliferation. Our finding suggests that FZD7 involved canonical Wnt signaling pathway is essential for tumorigenesis of TNBC. Thus, FZD7 may be a biomarker and a potential therapeutic target for triple negative breast cancer. 14 pretreatment non-triple negative breast tumors compare with 5 triple negative breast tumor.

2011-06-01 | E-GEOD-27447 | biostudies-arrayexpress

SOX2-OT induced by PAI-1 promotes triple-negative breast cancer cells metastasis

Project description:Triple-negative breast cancer (TNBC) has a relatively aggressive biological behavior and poor outcome. Our published study showed that PAI-1 could induce the migration and metastasis of TNBC cells. However, the underlying mechanism by which PAI-1 regulates TNBC metastasis has not been addressed. Using microarray analysis of lncRNA expression profiles, we identified a lncRNA SOX2-OT, which is by induced by PAI-1 and could function as an oncogenic lncRNA in TNBC.

2024-05-15 | GSE181202 | GEO

Comparative proteomics analysis of growth-primed adult dorsal root ganglia reveals key molecular mediators for peripheral nerve regeneration

Project description:Peripheral nerve injuries due to physical insults or chronic diseases are quite common, yet no pharmacological therapies are available for the effective repair of injured nerves. The slow growth rate of adult nerves and insufficient access to growth factors pose major hurdles in timely reinnervating target tissues and restoring functions after nerve injuries. A better understanding of the molecular changes that occur during the immediate regenerative reprogramming of neurons, stated here as in vivo priming, following nerve injury may reveal ideal candidates for future therapies. Hence, molecular profiling of neuronal soma within the first week of nerve injury has been the gold standard for revealing molecular candidates critical for nerve regeneration. A complementary in vitro regenerative priming approach was recently shown to induce enhanced outgrowth in adult sensory neurons. In this work, we exploited the in vitro priming model to reveal novel candidates for adult nerve regeneration. We performed the whole tissue proteomics analysis of in vitro primed DRGs and compared their molecular profile with that of the in vivo primed, and control DRGs. Through this approach, we identified several commonly and uniquely altered molecules in the in vitro and in vivo primed DRGs that have the potential to modulate adult nerve regrowth. We further validated the growth inducing potential of mesencephalic astrocyte-derived neurotrophic factor (MANF), one of the hits identified in our proteomics analysis, in primary adult sensory neurons. Overall, this study showed that in vitro priming partially reproduces the molecular features in in vivo primed adult sensory neurons. The shortlisted candidates presented here from the two priming approaches may serve as potential therapeutic targets for adult nerve regeneration.

2023-01-06 | PXD031927 | Pride

CDK7-dependent Transcriptional Addiction in Triple-Negative Breast Cancer (Microarray)

Project description:Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We postulate that TNBC might be highly dependent on uninterrupted transcription of a key set of genes within this gene expression program and might therefore be exceptionally sensitive to inhibitors of transcription. Utilizing a novel kinase inhibitor and CRISPR/Cas9-mediated gene editing, we show here that triple-negative but not ER/PR+ breast cancer cells are exceptionally dependent on CDK7, a transcriptional cyclin-dependent kinase. TNBC cells are unique in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition. An “Achilles cluster” of TNBC-specific genes are extremely sensitive to CDK7 inhibition and frequently associated with super-enhancers. We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in TNBC and CDK7 inhibition may be useful therapy for this challenging cancer. Expression microarrays in H3K27ac in triple-negative breast cancer +/- treatment with covalent CDK7 inhibitor THZ1 treatment

2015-09-24 | E-GEOD-69106 | biostudies-arrayexpress

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation III

Project description:While the inflammatory immune response of the lung to allergens and pathogens has been extensively studied, little is known about how sensory nerves change in response to an inflammatory insult within the organ they innervate. In our study we describe the collection of vagal sensory neurons innervating the mouse lung, labelled with a retrograde fluorescent tracer instilled into the airways, and the analysis of their transcriptomes by RNAseq. We also determined transcriptomes of the complete sensory ganglia (vagal, trigeminal, DRG) for comparison. We identified transcripts of genes exclusively expressed in vagal nerves, and not in any other sensory nerve type or any other organ. These include unique ion channels, G-protein coupled receptors and several transcripts of unknown function.

2020-03-15 | GSE141399 | GEO

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation II

2020-03-15 | GSE141395 | GEO

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation I

2020-03-15 | GSE141268 | GEO