Authors
Haokun Yang, Xin Nian
Published in
Molecular biology reports. Volume 53. Issue 1. Jun 30, 2026. Epub Jun 30, 2026.
Abstract
Breast cancer remains a highly heterogeneous malignancy in which metastasis and therapeutic resistance represent the primary drivers of patient mortality. Berberine (BBR), a natural isoquinoline alkaloid, has emerged as a promising pleiotropic agent capable of simultaneously targeting multiple oncogenic vulnerabilities. In this Review, we systematically outline the multifaceted molecular mechanisms underlying the anti-tumor efficacy of BBR in breast cancer. We detail how BBR disrupts core intracellular signaling networks-specifically the PI3K/AKT/mTOR, MAPK/ERK, and Wnt/β-catenin pathways-and modulates the m6A RNA epitranscriptome via the METTL3/IGF2BP3 axis to induce apoptosis, enforce cell cycle arrest, and suppress the epithelial-mesenchymal transition (EMT). Beyond direct cytotoxicity, we highlight BBR's capacity to remodel the tumor microenvironment (TME) by suppressing cancer-associated fibroblasts (CAFs) and tumor angiogenesis, while simultaneously targeting treatment-resistant cancer stem cells (CSCs) through the epigenetic restoration of tumor-suppressive microRNAs. Furthermore, we discuss the role of BBR as a potent chemosensitizer capable of reversing multidrug resistance to augment conventional chemotherapeutic and endocrine regimens. Finally, we address the inherent pharmacokinetic bottlenecks that limit BBR's clinical translation and examine how cutting-edge nanomedicine platforms can circumvent these barriers, offering a comprehensive translational roadmap for integrating BBR into next-generation oncology therapeutics.
PMID:
42377770
Bibliographic data and abstract were imported from PubMed on 30 Jun 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 6
- Comments 0