Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines via Inhibition of NF-κB and STAT3 Pathways

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  • Puthdee Nattapong
    Department of Biochemistry, Faculty of Medicine, Khon Kaen University Cholangiocarcinoma Research Institute, Khon Kaen University
  • Seubwai Wunchana
    Cholangiocarcinoma Research Institute, Khon Kaen University Department of Forensic Medicine, Faculty of Medicine, Khon Kaen University
  • Vaeteewoottacharn Kulthida
    Department of Biochemistry, Faculty of Medicine, Khon Kaen University Cholangiocarcinoma Research Institute, Khon Kaen University
  • Boonmars Thidarut
    Cholangiocarcinoma Research Institute, Khon Kaen University Department of Parasitology, Faculty of Medicine, Khon Kaen University
  • Cha’on Ubon
    Department of Biochemistry, Faculty of Medicine, Khon Kaen University Cholangiocarcinoma Research Institute, Khon Kaen University
  • Phoomak Chatchai
    Department of Biochemistry, Faculty of Medicine, Khon Kaen University Cholangiocarcinoma Research Institute, Khon Kaen University
  • Wongkham Sopit
    Department of Biochemistry, Faculty of Medicine, Khon Kaen University Cholangiocarcinoma Research Institute, Khon Kaen University

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  • Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines <i>via</i> Inhibition of NF-κB and STAT3 Pathways

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<p>Berberine is a natural compound found in several herbs. Anticancer activity of berberine was reported in several cancers, however, little is known regarding the effects of berberine against cholangiocarcinoma (CCA). In this study, the growth inhibitory effects of berberine on CCA cell lines and its molecular mechanisms were explored. Cell growth and cell cycle distribution were examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. The expression levels of cell cycle regulatory proteins were determined by Western blot analysis. Berberine significantly inhibited growth of CCA cell lines in a dose and time dependent fashion. The inhibition was largely attributed to cell cycle arrest at the G1 phase through the reduction of cyclin D1, and cyclin E. Moreover, berberine could reduce the expression and activation of signal transducers and activator of transcription 3 (STAT3) and probably nuclear factor-kappaB (NF-κB) via suppression of extracellular signal-regulated kinase (ERK) 1/2 action. These results highlight the potential of berberine to be a multi-target agent for CCA treatment.</p>

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