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LGR4 attenuates MGP expression and suppresses EGFR activation-induced triple-negative breast cancer metastasis
Qishuang Li1, Yankun Gao2, Zitian Huo3
1State Key Laboratory of Targeting Oncology, National Center for International Research of Biotargeting Theranostics, Guangxi Key Laboratory of Biotargeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Medical University Nanning 530021, Guangxi, PR China.
Abstract:
Breast cancer has emerged as the most common cancer globally, with a significant reduction in overall survival rate after metastasis. Compared with other types of breast cancer, triple-negative breast cancer (TNBC) is more prone to metastasize, presenting substantial treatment challenges due to the lack of effective therapies. LGR4, which is highly expressed in breast cancer, has been shown to promote the proliferation and invasion of breast cancer cells. However, its specific role in TNBC remains unclear. In this study, we applied a multi-omics approach to explore the regulatory mechanism of LGR4 in TNBC metastasis. Our findings showed that LGR4 could regulate actin cytoskeletal through EGFR and curtail EGFR activation-induced TNBC metastasis by inhibiting MGP expression. These insights provide new perspectives on the role of LGR4 in breast cancer metastasis.
Insights
Leucine-rich repeat-containing G-protein coupled receptor 4 (LGR4) promotes triple-negative breast cancer (TNBC) metastasis by regulating the actin cytoskeleton. This study reveals LGR4 inhibits MGP expression, curtailing EGFR activation-induced TNBC spread.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Breast cancer is the most common global cancer, with metastasis significantly reducing survival rates.
- Triple-negative breast cancer (TNBC) exhibits higher metastatic potential and limited therapeutic options.
- Leucine-rich repeat-containing G-protein coupled receptor 4 (LGR4) is overexpressed in breast cancer, promoting proliferation and invasion, but its role in TNBC metastasis is unclear.
Purpose of the Study:
- To elucidate the regulatory mechanism of LGR4 in triple-negative breast cancer (TNBC) metastasis using a multi-omics approach.
- To investigate the specific molecular pathways influenced by LGR4 in TNBC progression.
Main Methods:
- Application of a multi-omics approach to analyze LGR4 function in TNBC.
- Investigation of LGR4's interaction with the actin cytoskeleton and Epidermal Growth Factor Receptor (EGFR) signaling.
- Analysis of MGP (Matrix Gla Protein) expression regulation by LGR4.
Main Results:
- LGR4 was found to regulate the actin cytoskeleton in TNBC cells.
- LGR4 was shown to inhibit Epidermal Growth Factor Receptor (EGFR) activation-induced metastasis.
- LGR4 was identified to suppress Matrix Gla Protein (MGP) expression.
Conclusions:
- LGR4 plays a critical role in regulating TNBC metastasis through actin cytoskeleton modulation and EGFR signaling.
- Inhibition of MGP expression by LGR4 is a key mechanism curtailing EGFR-driven TNBC metastasis.
- These findings offer novel insights into LGR4's function and potential therapeutic targets for TNBC.
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