The N-butyl isothiocyanate inhibited breast cancer by suppressing MIF-CD74 interaction

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Breast cancer is a leading global malignancy in women.
• Triple-negative breast cancer (TNBC) presents a poor prognostic outcome.
• Isothiocyanate compounds (ITCs) are explored for therapeutic potential.

Purpose of the Study:

• To investigate the anti-breast cancer effects of BI.
• To elucidate the molecular mechanisms underlying BI's action.
• To evaluate BI's efficacy in a preclinical breast cancer model.

Main Methods:

• In vitro studies using MCF7 and 4T1 breast cancer cell lines.
• Analysis of cell proliferation, migration, apoptosis, and autophagy.
• Investigation of molecular targets including MIF, JAK2/STAT3, MEK/ERK, NF-κB, and ROS.
• In vivo studies using a 4T1 xenograft tumor model.

Main Results:

• BI inhibited proliferation and migration while promoting apoptosis and autophagy in breast cancer cells.
• BI suppressed the MIF-CD74 interaction, inhibiting JAK2/STAT3 signaling and downstream gene transcription.
• BI selectively inhibited MEK/ERK and NF-κB activation and increased ROS in 4T1 cells.
• BI reduced tumor weight and volume in vivo without systemic toxicity.

Conclusions:

• BI demonstrates significant anti-breast cancer activity.
• BI targets key signaling pathways involved in breast cancer progression.
• BI represents a potential novel therapeutic agent for breast cancer, particularly TNBC.