Berberine Inhibits MDA-MB-231 Cells by Attenuating Their Inflammatory Responses

Biomed Res Int. 2020 Mar 16:2020:3617514. doi: 10.1155/2020/3617514. eCollection 2020.

Abstract

Breast cancer initiation is closely associated with cytokines that can change the inflammatory tumor microenvironment. Compounds extracted from plants have been explored for the possibility of cancer treatment in the recent decades. Berberine is an isoquinoline plant alkaloid with remarkable antioxidant and anti-inflammation roles, which is used in ethnic medicines, including traditional Chinese and North American medicine. In the present study, we investigated the effects of berberine on the malignant tumor cell behaviors in a breast cell line, MDA-MB-231. We found that berberine could not influence the cell viability in normal condition but was able to decrease the cancer cell migration capability in a scratch wound model and accordingly prolong the wound healing time. Furthermore, our results demonstrated that berberine inhibited the increased phosphorylation of c-Jun and c-Fos in these scratched cancer cells. With the cotreatment with LPS, which could boost the expression of cytokines in these cancer cells, berberine significantly reduced the increased expression of TNF-α and IL-6. Meanwhile, we found that berberine inhibited the activation of NF-κB by preventing the degradation of IκBα.

MeSH terms

  • Alkaloids / pharmacology*
  • Antioxidants / pharmacology*
  • Berberine / pharmacology*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Inflammation / drug therapy
  • Inflammation / genetics
  • JNK Mitogen-Activated Protein Kinases / genetics
  • NF-KappaB Inhibitor alpha / genetics
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-fos / genetics
  • Signal Transduction / drug effects
  • Transcription Factor RelA / genetics
  • Tumor Microenvironment / drug effects
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Alkaloids
  • Antioxidants
  • Proto-Oncogene Proteins c-fos
  • RELA protein, human
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Berberine
  • NF-KappaB Inhibitor alpha
  • JNK Mitogen-Activated Protein Kinases