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A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
Published on: February 20, 2018
[Inhibitory effect of LRRC4 on the mobility and invasion of glioblastomas through the SDF-1alpha/CXCR4 axis]
Qiong Chen1, Ming-hua Wu, Yan-hong Zhou
1Cancer Research Institute, Central South University, Changsha 410078, China.
Objective:
To explore the effect of LRRC4 on the mobility and invasion of glioblastomas U251 cells through the SDF-1alpha/CXCR4 axis.
Methods:
RT-PCR, transfilter cell invasion assay, adhesion assay, scraping test, scrape loading, and dye transfer assay were used to determine the effect of LRRC4 on U251 cells.
Results:
SDF-1 alpha could increase the invasion in U251 which expressed CXCR4. The reintroduction of LRRC4 in U251 cells could inhibit the expression of CXCR4. LRRC4 also inhibited the adhesion ability of U251 to ECV304 as well as the mobility and invasion ability in vitro, which was mediated by the SDF-1alpha/CXCR4 axis. Furthermore, LRRC4 could greatly enhance the gap junctional intercellular communication of U251 cells.
Conclusion:
The reintroduction of LRRC4 in U251 cells can inhibit the expression of CXCR4 and the SDF-1alpha/CXCR4 axis-mediated cell invasion in vitro.
Insights
Leucine-rich repeat-containing protein 4 (LRRC4) inhibits glioblastoma cell invasion by downregulating CXCR4 expression and the SDF-1alpha/CXCR4 axis. LRRC4 also enhances intercellular communication in U251 cells.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cell Biology
Context:
- Glioblastoma multiforme (GBM) is an aggressive brain tumor with poor prognosis.
- The SDF-1alpha/CXCR4 signaling pathway plays a critical role in glioblastoma cell migration and invasion.
- Understanding the molecular mechanisms regulating glioblastoma progression is crucial for developing effective therapies.
Purpose:
- To investigate the role of Leucine-rich repeat-containing protein 4 (LRRC4) in regulating the mobility and invasion of U251 glioblastoma cells.
- To elucidate the involvement of the SDF-1alpha/CXCR4 axis in LRRC4-mediated effects on glioblastoma cells.
- To assess the impact of LRRC4 on U251 cell adhesion, migration, and invasion in vitro.
Summary:
- Reintroduction of LRRC4 into U251 glioblastoma cells significantly inhibited cell invasion and migration.
- LRRC4 was found to downregulate the expression of CXCR4, a key receptor in the SDF-1alpha/CXCR4 axis.
- LRRC4 suppressed U251 cell adhesion to ECV304 cells and enhanced gap junctional intercellular communication.
Impact:
- LRRC4 acts as a potential tumor suppressor in glioblastoma by inhibiting cell invasion and metastasis.
- Targeting the SDF-1alpha/CXCR4 axis, potentially modulated by LRRC4, could offer a therapeutic strategy for glioblastoma.
- The findings highlight LRRC4's multifaceted role in regulating glioblastoma cell behavior and intercellular communication.
