mProX™ Human GPR87 Stable Cell Line

Product Information

Target Protein

GPR87

Target Family

Orphan Family

Target Protein Species

Human

Host Cell Type

A549;H1299;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

Cancer Research

Related Diseases

Squamous Cell Carcinoma;Lung Squamous Cell Carcinoma

Gene ID

Human: 53836

UniProt ID

Human: Q9BY21

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

GPR87 has been identified as a significant factor in various cancers. In lung adenocarcinoma, GPR87 promotes tumor progression and is associated with immune infiltration, suggesting its potential as a prognostic biomarker. Furthermore, GPR87 has been linked to renal fibrosis, where it accelerates glycolysis and mitochondrial injury. This receptor has also been associated with homeostatic signaling in the context of lacritin, a protein involved in tear production and eye health.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Linda (Verified Customer)

How does GPR87 overexpression relate to cancer progression in cell lines? Jul 07 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

GPR87 overexpression has been linked to the promotion of cell proliferation in lung cancer cell lines. This suggests that GPR87 could serve as a potential biomarker or therapeutic target in cancer treatment, with stable cell lines aiding in the investigation of these prospects. Jul 07 2021

chat Karen (Verified Customer)

What role does GPR87 play in cell line-based cancer research? Jul 21 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

GPR87's role in cancer cell lines, particularly its overexpression in lung cancer cells, helps in understanding its potential as a therapeutic target. Its association with cell proliferation provides a platform for studying the molecular mechanisms underlying cancer progression. Jul 21 2020

Published Data

Fig.1 GPR87 knockdown prevents the formation of LUAD cells.

The clone formation assay results revealed a notable reduction in cell proliferation for both A549 and H1299 cells upon GPR87 knockdown, with statistical significance at *p<0.05.

Ref: Bai, Rui, et al. "GPR87 promotes tumor cell invasion and mediates the immunogenomic landscape of lung adenocarcinoma." Communications Biology 5.1 (2022): 663.

Pubmed: 35790819

DOI: 10.1038/s42003-022-03506-6

Research Highlights

Sun H, et al. "Prognostic evaluation of pancreatic cancer based on the model of ." Journal of gastrointestinal oncology, 2023.
The incidence and mortality rates of pancreatic cancer are comparable, with a low 5-year survival rate of less than 10%. A key factor contributing to the high mortality of this cancer is its resistance to chemo-radiotherapy. To address this issue, the current study aimed to develop a prognostic model for pancreatic cancer, utilizing chemo-radiotherapy resistant-related genes (CRRGs). Through investigating radiation- and gemcitabine-resistant pancreatic cancer cell lines and utilizing data from the Gene Expression Omnibus database, a model consisting of nine CRRGs (SNAP25, GPR87, DLL1, LAD1, WASF3, ARHGAP29, ZBED2, GAD1, and JAG1) was established and validated using data from The Cancer Genome Atlas and the GEO database. Further analysis revealed that these genes played a crucial role in promoting the proliferation and chemo-radiotherapy tolerance of pancreatic cancer cells, particularly JAG1, which has been linked to the maintenance of cancer cell stemness. The results of this study suggest that targeting CRRGs, particularly JAG1, may serve as a promising approach to improve the prognosis of pancreatic cancer patients.
Pubmed: 37435207 DOI: 10.21037/jgo-23-308

Liu Q, et al. "The Genetic Landscape of Familial Pulmonary Fibrosis.." American journal of respiratory and critical care medicine, 2023.
In this study, Wu et al. aimed to investigate the genetic risk factors for familial pulmonary fibrosis (FPF) by analyzing rare genetic variants in a large cohort of FPF kindreds. Whole-exome sequencing and/or candidate gene sequencing was performed on affected individuals from 569 FPF families. The results revealed that 14.9-23.4% of FPF genetic risk was attributed to rare variants in telomere-related genes. Additionally, several new candidate genes were identified, including SYDE1, SERPINB8, GPR87, and NETO1. Pathway analysis showed enrichment of these variants in genes associated with focal adhesion and mitochondrial complex I assembly. Single-cell transcriptomics further highlighted the expression of rare variant-containing genes in specific cell types. These findings suggest that a heterogeneous pool of genetic variants in various genes and pathways contributes to genetic risk in most FPF kindreds. This study provides comprehensive insight into the genetic basis of FPF and identifies potential targets for further research.
Pubmed: 36622818 DOI: 10.1164/rccm.202204-0781OC