Targeting STAT3 in Breast Cancer Using Innovative Natural and Synthetic Scaffolds to Trigger Apoptosis, Autophagy,...

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Signal Transducer and Activator of Transcription 3 (STAT3) is crucial in breast cancer (BC) progression, driving proliferation, metastasis, survival, and chemoresistance.
• STAT3 phosphorylation at tyrosine 705 activates oncogenic pathways, making it a key therapeutic target in BC.

Purpose of the Study:

• To synthesize, characterize, and evaluate synthetic and natural compounds for their ability to inhibit STAT3 phosphorylation.
• To assess the efficacy of these compounds in suppressing breast cancer cell proliferation, inducing apoptosis, and promoting autophagy.

Main Methods:

• A comprehensive literature review was performed using PubMed, Scopus, Relemed, and ResearchGate.
• Studies focusing on STAT3 inhibitors, including synthetic derivatives and phytochemicals, were analyzed for their molecular mechanisms and therapeutic potential in breast cancer.

Main Results:

• Various synthetic and natural compounds effectively inhibited STAT3 phosphorylation, reducing breast cancer cell proliferation, migration, and survival.
• These compounds induced apoptosis and autophagy, demonstrating multifaceted anti-tumor activity and potential as lead candidates for further development.

Conclusions:

• Targeting STAT3 with synthetic or natural compounds represents a significant therapeutic strategy for breast cancer, supported by preclinical evidence.
• These findings offer valuable insights for researchers and clinicians exploring STAT3 inhibitors as novel breast cancer therapeutics.