GPRC5A regulates keratinocyte adhesion and migration through nuclear translocation of its C-terminus region
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1043579 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26898690.fastq.gz | Fastqsanger.gz | |||
| SRR26898691.fastq.gz | Fastqsanger.gz | |||
| SRR26898692.fastq.gz | Fastqsanger.gz | |||
| SRR26898693.fastq.gz | Fastqsanger.gz | |||
| SRR26898694.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:G-Protein Coupled Receptor, Class C, Group 5, Member A (GPRC5A) is well-documented in lung and various epithelial cancers. However, its role in the skin remains unexplored. In this study, we investigated the function of this receptor in skin biology and our research demonstrated that its expression responds to mechanical substrate changes in human primary keratinocytes. Furthermore, we observed GPRC5A reinduction during wound healing at the leading edges in an ex vivo burn model, coinciding with the translocation of its C-terminal region into the nucleus. We identified the cleavage site of GPRC5A by N-TAILS analysis, and cathepsin G was characterized as responsible for proteolysis in cultured cells. To gain a deeper understanding of GPRC5A's role in keratinocyte, we performed GPRC5A knockdown in N/TERT-1 cells using short-hairpin RNA. Our findings strongly suggest a close association between GPRC5A and adhesion regulation pathways, but also demonstrate that GPRC5AKD enhanced cell adhesion while reducing cell migration and differentiation. Importantly, these effects were reversed by adding a recombinant polypeptide mimicking the C-terminal region of GPRC5A. Overall, our study reveals an unexpected role of GPRC5A in regulating keratinocyte behavior, implicating its C-terminal region translocation into the nucleus. These results open up interesting strategic pathways for wound healing.
2023-11-27 | GSE248355 | GEO
Project description:Transcriptional profiling of HeLa cervical carcinoma cells comparing cells with siRNA- or shRNA-mediated depletion of GPRC5A vs. cells carrying non-targeting siRNA or shRNA after 45 min and 6 h of adhesion to 10% Matrigel matrix. The goal was to determine the effect of GPRC5A depeltion on the global gene expression following the adhesion process.
2016-12-31 | GSE68338 | GEO
Project description:Gprc5a is a lung tumor suppressor gene. Gprc5a-knockout (ko) mice can develop spontaneous lung cancer and Gprc5a-ko mouse model is relevant to human lung cancer. Thus, exploration of the mechanisms underlying lung tumorigenesis in Gprc5a-ko mice would be very helpful for revealing those in human lung cancer. We used microarrays to detail the global gene expression profile that underlies oncogenesis by Gprc5a-knockout gene deletion in mouse tracheal epithelial cells. Wild type and gene-knockout mouse tracheal epithelial cells that were divided into two groups were used for RNA extraction.
2013-10-29 | E-GEOD-51777 | biostudies-arrayexpress
Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Gprc5a wild type cells (WT-NLE) and Gprc5a knockout cells (NULL-NLE) were isolated and cultured from trachea of three week old Gprc5a wild type and knockout mice, respectively. Following RNA extraction and purification, the transcriptome of the Gprc5a wild type and knockout cells were analyzed by microarray analysis using the Affymetrix MG-430 2.0 murine array platform.
2010-04-13 | E-GEOD-21309 | biostudies-arrayexpress
Project description:We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure.
2021-03-19 | GSE147148 | GEO
Project description:Gprc5a is a lung tumor suppressor gene. Gprc5a-knockout (ko) mice can develop spontaneous lung cancer and Gprc5a-ko mouse model is relevant to human lung cancer. Thus, exploration of the mechanisms underlying lung tumorigenesis in Gprc5a-ko mice would be very helpful for revealing those in human lung cancer. We used microarrays to detail the global gene expression profile that underlies oncogenesis by Gprc5a-knockout gene deletion in mouse tracheal epithelial cells.
2013-10-29 | GSE51777 | GEO
Project description:Galectins, a family of glycan-binding proteins, play crucial roles in various cellular functions, acting both at intracellular and extracellular levels. Among them, Galectin-3 (Gal-3) stands out as a unique member, belonging to the chimera subfamily. Gal-3 recruitment of plasma membrane glycosylated cargo leads to clustering and membrane bending, ultimately resulting in the formation of endocytic invaginations. An interactomic analysis on endogenous Gal-3 identified the orphan G-protein coupled receptor GPRC5A as a new binding partner for Gal-3. GPRC5A is also termed RAI3 as its expression is induced by retinoic-acid. Our results also show that GPRC5A is internalized by addition of extracellular Gal-3 and that GPRC5A trafficking pathway goes via the early and the recycling endosomes. In SW480 colorectal cancer cells, the glycosylated forms of GPRC5A interact with Gal-3 and their levels were increased by all-trans retinoic-acid (ATRA) addition. In SW480 cells, endocytic internalization of endogenous GPRC5A was achieved by extracellular Gal-3 addition but not by ATRA. This study reveals insights into the endocytic mechanisms of GPRC5A for which no specific ligand is described. Further research in this direction may unveil additional Gal-3 mediated functions in GPRC5A cellular signaling and contribute to the development of innovative therapeutic approaches.
2025-10-09 | PXD048507 | Pride
Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Moreover, we analyzed differential gene expression patterns between Gprc5a knockout normal lung epithelial cells as well as lung adenocarcinoma cells isolated and cultured from tumors of NNK-exposed Gprc5a knockout mice.
2010-04-13 | GSE21309 | GEO
Project description:Prostate cancer is a high frequent disease. Early stage prostate cancer can be cured with high probability by early treatment, but hormone refractory prostate cancer and progressive prostate cancer is poor prognosis. Orphan GPCRs have the potential to become a drug discovery target in various carcinomas, but there are few reports in prostate cancer and there are still many possibilities. By big data analysis, we focused on the biological properties of the prostate cancer cell line and found GPRC5A from Orphan GPCR as one of the regulators of prostate cancer development. GPRC5A knock out by genomic editing in PC3, proliferative ability and bone metastasis was markedly suppressed. In prostate cancer cells, GPRC5A inhibit phosphorylation of CREB and affected the expression of cell cycle related genes. GPRC5A is also involved in the establishment of bone metastases, and correlated with prostate cancer metastasis and prognosis. These dates suggest that GPRC5A facilitates cell proliferation and progression of prostate cancer and can be a target for new prognostic marker or drug discovery of prostate cancer.
2019-07-16 | GSE121319 | GEO
Project description:The clearance of oxidative stress compounds is critical for the protection of the organism from malignancy, but how this key physiological process is regulated is not fully understood. Here we found that the expression of GPRC5A, a well-characterized tumor suppressor in lung cancer, was elevated in colorectal cancer tissues in patients. In both cancer cell lines and a colitis-associated cancer model in mice, we found that GPRC5A deficiency reduced cell proliferation and increased cell apoptosis as well as inhibited tumorigenesis in vivo. Through RNA-Seq transcriptome analysis, we identified oxidative stress associated pathways were dysregulated. Moreover, in GPRC5A deficient cells and mouse tissues, the oxidative agents were reduced partially due to increased glutathione (GSH) level. Mechanistically, GPRC5A regulates NF-κB mediated Vanin-1 expression which is the predominant enzyme for cysteamine synthesis. Administration of cystamine (the disulfide form of cysteamine) in GPRC5A deficient cell lines inhibited γ-GCS activity leading to restoration of GSH level and increase of cell growth. Taken together, our studies suggest that GPRC5a is a potential biomarker for colon cancer and promotes tumorigenesis through stimulation of Vanin-1 expression and oxidative stress in colitis associated cancer. This study revealed an unexpected oncogenic role of GPRC5A in colorectal cancer suggesting there are complicated functional and molecular mechanism differences of this gene in distinct tissues.
2016-09-14 | GSE86895 | GEO