CCNL1 Activates the NF-κB Pathway Through DVL3 Inhibition and PI3K/AKT Pathway Promotion in Breast Cancer

Area of Science:

• Oncology
• Molecular Biology
• Cell Biology

Background:

• Cyclin L1 (CCNL1) is overexpressed in various cancers, correlating with poor prognosis.
• The role of CCNL1 in breast cancer progression and its underlying mechanisms are not well understood.

Purpose of the Study:

• To investigate the expression pattern and function of CCNL1 in breast cancer.
• To elucidate the molecular mechanisms by which CCNL1 regulates breast cancer cell proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT).

Main Methods:

• Plasmid transfection, Transwell and wound-healing assays for cell behavior analysis.
• Western blot, co-immunoprecipitation (Co-IP), and rescue assays for molecular interactions.
• Bioinformatics analysis using Metascape and HURI for pathway analysis.

Main Results:

• CCNL1 overexpression enhances breast cancer cell invasion, migration, and proliferation.
• CCNL1 upregulates Vimentin and downregulates E-cadherin, indicating EMT promotion.
• CCNL1 interacts with DVL3 and activates NF-κB and PI3K/AKT signaling pathways.

Conclusions:

• CCNL1 plays a significant role in breast cancer progression.
• CCNL1 promotes EMT and influences chemoresistance through NF-κB and PI3K/AKT signaling.
• CCNL1 represents a potential therapeutic target for breast cancer treatment.