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Overexpression of b-Arrestins in triple negative breast cancer cells.

ABSTRACT: Beta-Arrestins (βArrs) are intracellular signal regulating proteins. Their expression level varies in some cancers and they have significant impact on cancer cell function. In general, the significance of βArrs in cancer research comes from studies examining GPCR signalling. Given the diversity of different GPCR signals in cancer cell regulation, contradictory results are inevitable regarding the role of βArrs. Our approach examines the direct influence of βArrs on cellular function and gene expression profiles by changing their expression levels in breast cancer cells, MDA-MB-231.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156802 | GEO | 2021/01/15

REPOSITORIES: GEO

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Exploring GPCR-arrestin interfaces with genetically encoded crosslinkers

Project description:-arrestins (arr1 and arr2) are ubiquitous regulators of G protein-coupled receptor (GPCR) signalling. Available data suggest that -arrestins dock to different receptors in different ways. However, the structural characterization of arrestin-GPCR complexes is challenging and alternative approaches to study arrestin-GPCR complexes are needed. Here, starting from the finger loop as a major site for the interaction of arrestins with GPCRs, we genetically incorporate non-canonical amino acids for photo- and chemical crosslinking into arr1 and arr2 and explore binding topologies to GPCRs forming either stable or transient complexes with arrestin: the vasopressin receptor 2 (rhodopsin-like), the corticotropin releasing factor receptor 1 and the parathyroid hormone receptor 1 (both secretin-like). We show that each receptor leaves a unique footprint on arrestin, whereas the two -arrestins yield quite similar crosslinking patterns. Furthermore, we show that the method allows defining the orientation of arrestin respect to the GPCR. Finally, we provide direct evidence for the formation of arrestin oligomers in the cell.

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Beta arrestin1 associated genomic regions in nicotine induced Non-Small Cell Lung Carcinoma (NSCLC) cell line A549

Project description:The multifunctional scaffolding protein β-arrestin-1 plays a vital role in mediating the proliferative effects of nicotine through nAChR signaling. β-arrestins were initially known as negative regulators of GPCR mediated signaling as they promote internalization and desensitization of GPCRs. However, new roles of β-arrestins in receptor trafficking and signaling have been discovered in recent years. They are known to regulate signaling through a number of receptors such as Notch, endothelin A receptor, frizzled, smoothened and the nicotinic cholinergic receptors. Studies from our lab revealed that nAChR signaling induces the translocation of β-arrestin-1 to the nucleus, in a Src dependent manner, where it directly binds to the proliferative E2Fs. Furthermore, the nuclear translocation of β-arrestin-1 results in recruitment of p300 to E2F1 regulated proliferative promoters facilitating histone acetylation and transcription of these promoters. Given the role of β-arrestin-1 in nicotine induced gene expression, we attempted to explore the global association of β-arrestin-1 to the genomic regions upon nicotine stimulation by ChIP sequencing. It was found that β-arrestin-1 is recruited on the promoters of many genes that regulate EMT as well as other regulatory pathways. In this assay, β-arrestin-1 was found to be associated with the promoter regions of genes such as ZNF768, ZNF131, CSF3R, HMGA2, TAL1, RCC1, NKX2-4 etc in response to nicotine stimulation.

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