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PubMed · 42726146

Berberine shows potential in mitigating PM2.5-induced breast cancer progression by inducing DNA damage and inhibiting error-prone DNA repair pathways.

Anadi Bisht·Aishwarya Jaiswal·Rana P Singh·Sagnik Dey·Ritu Kulshreshtha
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Abstract

Breast cancer remains the most common cancer among women, with 2.3 million new cases reported globally in 2022. Alongside established risk factors such as age, family history, genetics, obesity, smoking, and alcohol, exposure to fine particulate matter (PM2.5) has recently emerged as an environmental contributor. This risk is especially concerning for low- and middle-income countries (LMICs), where both PM2.5 exposure and cancer burden are disproportionately high; however, mechanistic studies from these regions remain limited. To address this gap and develop mitigation strategies, we investigated the oncogenic potential of water-soluble PM2.5 collected from ambient air on breast cancer and evaluated the potential role of nutraceuticals in mitigating these effects. PM2.5 exposure increased proliferation, migration, and ROS generation, while promoting the formation of multinucleated giant cells, leading to genomic instability. Berberine, a natural alkaloid, countered these effects by increasing DNA damage and exploiting tumor-specific genomic vulnerabilities through disruption of DNA damage response and repair networks, thereby promoting programmed cell death. Transcriptomic profiling of Delhi PM2.5-treated MCF7 cells revealed a Delhi PM2.5-associated carcinogenic gene signature enriched in MAPK signalling, reactive oxygen species, metabolic, lysosomal, and ribosomal pathways. We also found that several genes, including BIRC5, WSB1, and RCC1, within this PM2.5-induced gene signature were dysregulated in breast cancer patients and were inversely regulated by berberine treatment, suggesting that berberine counteracts the transcriptional effects of PM2.5. Our findings highlight ambient PM2.5 exposure as a driver of breast cancer progression and identify berberine as a promising candidate in mitigating PM2.5 effects; however, thorough preclinical and clinical validations are warranted.

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BerberineHumansFemaleDNA DamageBreast NeoplasmsDNA RepairParticulate MatterCell ProliferationReactive Oxygen SpeciesApoptosisDisease ProgressionAir pollutionBreast cancerMitigation strategiesPM2.5Therapeutic nutraceuticalsJournal Article

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Anadi Bisht, Aishwarya Jaiswal, Rana P Singh, Sagnik Dey, Ritu Kulshreshtha. 2026-09-11. Berberine shows potential in mitigating PM2.5-induced breast cancer progression by inducing DNA damage and inhibiting error-prone DNA repair pathways.. https://doi.org/10.1007/s10495-026-02423-x

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PubMed2025

Network pharmacology approach to unveiling the mechanism of berberine in the amelioration of morphine tolerance.

OBJECTIVE: To investigate the mechanism underlying the effect of the Huanglian decoction (, HLD) on morphine tolerance (MT), using network pharmacology, and to verify these mechanisms in vitro and in vivo. METHODS: Available biological data on each drug in the HLD were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. The target proteins of MT were retrieved from the GeneCards, PharmGkb, Therapeutic Target Database, DrugBank, and Online Mendelian Inheritance in Man databases. Information regarding MT and the drug targets was compared to obtain overlapping elements. This information was imported into the Search Tool for the Retrieval of Interacting Genes/Proteins platform to obtain a protein-protein interaction network diagram. Then, a "component-target" network diagram was constructed using screened drug components and target information, viaCytoscape (Institute for Systems Biology, Seattle, WA, USA). The database for annotation, visualization, and integrated discovery was used for Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathways analyses. Pathway information predicted by network pharmacology was verified using animal studies and cell experiments. RESULTS: Network pharmacology analysis identified 22 active compounds of HLD and revealed that HLD partially ameliorated MT by modulating inflammatory, apoptosis, and nuclear factor kappa B (NF-κB) signaling pathways. Berberine (BBR), one of the main components of HLD, inhibited the development of MT in mice. BBR reduced cell viability while increasing B-cell lymphoma 2 (Bcl-2) protein expression and decreasing CD86, NF-κB, Bax, and Caspase-3 protein expression in brain vascular 2 (BV2) mcroglia cells treated with morphine. Additionally, BBR contributed to a reduction in pro-inflammatory cytokine release and apoptotic cell number. CONCLUSIONS: BBR, a key component of HLD, effectively suppressed microglial activation and neuro-inflammation by regulating the NF-κB and apoptosis signaling pathways, thereby delaying MT. This study offers a novel approach to enhance the clinical analgesic efficacy of morphine.

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