Novel therapy for locally advanced triple-negative breast cancer

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Triple-negative breast cancer (TNBC) presents a significant therapeutic challenge.
• Understanding novel treatment mechanisms is crucial for advancing breast cancer care.

Purpose of the Study:

• To evaluate vitamin K3 (VK3) as a potential therapeutic agent for TNBC.
• To elucidate the molecular pathways involved in VK3's anti-cancer effects.

Main Methods:

• In vitro studies utilized MTT assays and western blotting to assess VK3's impact on human breast cancer cell lines.
• In vivo studies involved a subcutaneous mouse tumor model treated with VK3 to measure tumor growth inhibition.
• Analysis included IC50 determination, assessment of protein phosphorylation (tyrosine, epidermal growth factor receptor, ERK, JNK), and comparison with catalase.

Main Results:

• VK3 demonstrated dose-dependent inhibition of breast cancer cell growth with an IC50 range of 11.3-25.1 µM.
• VK3 induced phosphorylation of tyrosine, epidermal growth factor receptor, ERK, and JNK, with sustained ERK activation.
• Local VK3 treatment significantly reduced tumor volume in mice in a time- and dose-dependent manner, with increased phosphorylated ERK expression in tumor tissue.

Conclusions:

• Extracellular signal-regulated kinase (ERK) plays a critical role in VK3-induced growth inhibition in TNBC.
• VK3 shows promise as a targeted molecular therapy for TNBC, warranting further investigation.
• The ERK pathway is a key target for future therapeutic development in TNBC treatment.