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

Breast cancer ranks as the most common malignant tumor in women across the globe, and triple-negative breast cancer (TNBC) has the worst prognostic outcome among all its molecular subtypes. In the present study, we found that BI exerted inhibitory effects on cell proliferation and migration, triggered cellular apoptosis, and also promoted autophagic activity in both MCF7 and 4T1 breast cancer cell lines. Further investigations suggested that BI likely targeted MIF and disrupted the MIF-CD74 interaction, thereby suppressing activation of JAK2/STAT3 signaling axis and transcription of downstream genes such as Il-6 and Socs3. Notably, BI inhibited MEK/ERK and NF-κB activation while increasing ROS levels specifically in 4T1 cells, but not in MCF7 cells. In a 4T1 xenograft tumor model, BI reduced tumor weight and volume without affecting body weight or major organ integrity. To summarize, our research provides the first documentation of the anti-breast cancer effects exerted by BI, laying a foundation for further exploration of isothiocyanate compounds (ITCs) as a potential source of novel therapeutic agents against breast cancer.