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  • br The increased e ectiveness of some

    2020-03-24


    The increased effectiveness of some of the NAX compounds in inhibiting proliferation could be due to multiple mechanisms. Some of the NAX compounds could induce more DNA damage than other which could result in cell death. Some of the NAX compounds
    Fig. 6. Effects of the Nutraceuticals Berberine And NAX Compounds on the Proliferation and IC50s of MIA-PaCa-2 + WT-TP53 (Adh.) Cells. Panel A) MTT analysis of MIA-PaCa-2 + WT-TP53 (Adh.) Latrunculin A plated with the different NAX compounds. In Panel B, the IC50s are presented graphically. All of the experiments indicated in this figure were performed on the same day. These experiments were repeated 6 times and similar results were obtained.
    Table 4 Effects of berberine and NAX compounds on MIA-PaCa-2 + WT-TP53 (Adh.) cells.a
    Compound IC50
    a Determined by MTT Analysis as presented in Abrams et al. (2018).
    could induce more ROS than others which would stimulate the induction of apoptosis. The induction of autophagy is also a possible mechanism which could explain the differences of the NAX compounds effectiveness. Elucidation of the mechanisms by which the different NAX compounds inhibit proliferation could further the usage of modified BBRs (NAX compounds) in cancer therapy as well as other diseases.
    Conflicts of interest
    The authors declare that they have no conflicts of interest with publication of this manuscript.
    Acknowledgements
    References
    Zhao, Y., Jing, Z., Li, Y., Mao, W., 2016. Berberine in combination with cisplatin suppresses breast cancer cell growth through induction of DNA breaks and caspase-3-dependent apoptosis. Oncol. Rep. 36, 567–572.
    182 Advances in Biological Regulation xxx (xxxx) xxxx
    Contents lists available at ScienceDirect
    Advances in Biological Regulation
    journal homepage: www.elsevier.com/locate/jbior
    Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells
    Shaw M. Akulaa,∗,1, Saverio Candidob,c,1, Massimo Librab,c, Stephen L. Abramsa, Linda S. Steelmana, Kvin Lertpiriyapongd, Giulia Ramazzottie, Stefano Rattie, Matilde Y. Folloe, Alberto M. Martellie, Ramiro M. Murataa,f, Pedro L. Rosaleng, Bruno Bueno-Silvag,h, Severino Matias de Alencari, Giuseppe Montaltoj,k, Melchiorre Cervellok, Agnieszka Gizakl, Dariusz Rakusl, Weifeng Maom, Heng-Liang Linn, Paolo Lombardio, James A. McCubreya,∗∗ a Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, 27858, USA
    b Department of Biomedical and Biotechnological Sciences – Oncological, Clinical and General Pathology Section, University of Catania, Catania, Italy cResearch Center for Prevention, Diagnosis and Treatment of Cancer (PreDiCT), University of Catania, Catania, Italy d Center of Comparative Medicine and Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine and the prothallus Hospital for Special Surgery, New York City, New York, USA e Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy
    f Department of Foundational Sciences, School of Dental Medicine, East Carolina University, USA
    g Department of Physiological Sciences, Piracicaba Dental School, State University of Campinas, Piracicaba, Brazil
    h Dental Research Division, Guarulhos University, Guarulhos, Brazil
    i Universidade de São Paulo - USP, “Luiz de Queiroz” College of Agriculture, São Paulo, Brazil
    j Dipartimento di Promozione Della Salute, Materno-Infantile, Medicina Interna e Specialistica di Eccellenza (PROMISE), University of Palermo, Palermo, Italy
    k Consiglio Nazionale Delle Ricerche, Istituto di Biomedicina e Immunologia Molecolare “Alberto Monroy”, Palermo, Italy
    l Department of Molecular Physiology and Neurobiology, Wroclaw University, Wroclaw, Poland
    m College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China