mProX™ Human LPAR3 Stable Cell Line

Product Information

Target Protein

LPAR3

Target Family

Lysophospholipid Family

Target Protein Species

Rat

Host Cell Type

WB-F344;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

Cancer Research

Related Diseases

Trachea Adenoid Cystic Carcinoma;Tracheal Cancer

Gene ID

Rat: 66025

UniProt ID

Rat: Q8K5E0

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

LPAR3 has been associated with various cancer-related processes. Circular RNA lysophosphatidic acid receptor 3 (circ-LPAR3) has been shown to enhance the cisplatin resistance of ovarian cancer. Additionally, LPAR3 has been identified as playing a role in promoting tumor progression in Ras-transformed cells through autophagy induction. In the context of esophageal cancer, circular RNA LPAR3 has been implicated in promoting cell migration, invasion, and metastasis. Furthermore, LPAR3 has been linked to the regulation of inflammation in human IL-1β-stimulated fibroblast-like synoviocytes and carrageenan/kaolin-induced arthritis in rats.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Elizabeth (Verified Customer)

What is the role of the ATX-LPA signaling in breast cancer cell lines? Oct 31 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

ATX-LPA signaling has a dose-dependent stimulatory effect, especially on the cellular functions of triple-negative and luminal A breast cancer cell lines. This might contribute to identifying subtypes suitable for a future targeted therapy of the ATX-LPA axis. Oct 31 2022

chat Elizabeth (Verified Customer)

How does Circular RNA LPAR3 influence esophageal cancer? Jun 28 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

Circular RNA LPAR3 can regulate the miR-198-MET signal axis to promote the migration, invasion, and metastasis of esophageal cancer cells. This suggests it could serve as a potential diagnostic and therapeutic target for esophageal cancer. Jun 28 2020

Published Data

Fig.1 In WB-shRNA3-2 cells, the potent induction of cell motility triggered by hydrogen peroxide was effectively nullified, resulting in the complete inhibition of Lpar3 expression.

The transcript abundance of the Lpar3 gene and cellular migratory capacity were assessed in WB-shRNA3-2 cells exposed to hydrogen peroxide for 48 hours. Columns represent the average of three experiments, with error bars denoting standard deviation. ∗ p < 0.01 compared to untreated (control) cells.

Ref: Shibata, Ayano, et al. "Hydrogen peroxide stimulates cell motile activity through LPA receptor-3 in liver epithelial WB-F344 cells." Biochemical and Biophysical Research Communications 433.3 (2013): 317-321.

Pubmed: 23510996

DOI: 10.1016/j.bbrc.2013.02.100

Research Highlights

Yu H, et al. "AP003352.1/miR-141-3p axis enhances the proliferation of osteosarcoma by LPAR3.." PeerJ, 2023.
The research discussed in this abstract focuses on Osteosarcoma (OS), a highly malignant tumor with a poor prognosis and a growing incidence. The study explores the role of long non-coding RNAs (lncRNAs) and microRNAs in the development of OS through a competitive endogenous RNA (ceRNA) mechanism. Specifically, the regulatory mechanism of the ceRNA network involving the LPAR3 gene in OS has not yet been fully understood. Through their study, the authors demonstrate that the AP003352.1/miR-141-3p axis plays a crucial role in driving LPAR3 expression and promoting the malignant progression of OS. The relationship between AP003352.1 and miR-141-3p is similar to that of a ceRNA, as both regulate LPAR3 expression. Moreover, the regulation of AP003352.1 in OS progression is partly dependent on miR-141-3p. The authors identify the AP003352.1/miR-141-3p/LPAR3 axis as a potential multi-gene diagnostic marker for OS and propose it as a novel target for OS treatment.
Pubmed: 37727685 DOI: 10.7717/peerj.15937

Heo SC, et al. "Lysophosphatidic acid induces proliferation and osteogenic differentiation of ." Journal of dental sciences, 2023.
The present study aimed to investigate the impact of lysophosphatidic acid (LPA) signaling on the proliferation and osteogenic differentiation of human dental pulp stem cells (hDPSCs). Utilizing the cell counting kit-8 assay, the researchers assessed the proliferation of hDPSCs treated with LPA. Osteoblast differentiation was induced in hDPSCs through osteogenic medium, with and without LPA, and subsequently analyzed through alkaline phosphatase (ALP) staining, ALP activity measurements, and RT-qPCR. Additionally, LPAR3-specific siRNA and extracellular signal-regulated kinase (ERK)/mitogen-activated protein (MAP) kinase inhibitors were employed to better understand the underlying molecular mechanisms of LPA-induced proliferation and differentiation in hDPSCs. The results showed that LPA treatment significantly increased both proliferation and osteogenic differentiation in hDPSCs. Gene silencing of LPAR3 using LPAR3-specific siRNA greatly reduced the effects of LPA on proliferation and differentiation. Furthermore, U0126, a selective inhibitor of ERK, significantly decreased the LPAR3-mediated proliferation and osteogenic differentiation of hDPSCs induced by LPA. Therefore, it can be concluded that LPA promotes the proliferation and osteogenic differentiation of hDPSCs through LPAR3-ERK-dependent pathways.
Pubmed: 37404649 DOI: 10.1016/j.jds.2023.01.029