Abstract PS2-11-10: Mct4 drives triple-negative breast cancer progression via lactate-induced histone lactylation and mapk pathway activation

Key Points

• This research aims to clarify the role of Mct4 in the progression of triple-negative breast cancer (TNBC) and its implications for therapy.
• Analyzed MCT4 expression in TNBC tissues and its correlation with clinical outcomes.
• Performed hypoxia treatment and paclitaxel exposure on MDA-MB-231 cells, followed by MCT4 knockdown via siRNA.
• Conducted in vivo xenograft experiments to assess tumor growth and drug response.
• Utilized RNA-sequencing and KEGG pathway analysis to explore gene expression changes.
• Measured lactate secretion, glucose uptake, and Western blot analysis of MAPK pathway proteins.
• MCT4 was overexpressed in TNBC tissues, correlating with poor patient prognosis.
• Knockdown of MCT4 inhibited cell proliferation, invasion, and migration while increasing sensitivity to paclitaxel.
• In vivo studies revealed MCT4 knockdown significantly slowed tumor growth and enhanced treatment response.
• RNA-sequencing indicated that MCT4 knockdown reduced MAPK signaling pathway activity.
• Histone lactylation modifications were affected by MCT4 knockdown, linking lactate metabolism to gene regulation.