Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells

Anticancer Res. 2021 Dec;41(12):5919-5933. doi: 10.21873/anticanres.15411.

Abstract

Background/aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells.

Materials and methods: DATS efficacy on TNF-α induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR.

Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-κB and MAPK signaling.

Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.

Keywords: Breast cancer; CCL2; IKBKE; MAPK8; MCP-1; diallyl trisulfide; tumor necrosis factor alpha.

MeSH terms

  • Allyl Compounds / pharmacology*
  • Apoptosis / drug effects
  • Biomarkers, Tumor / metabolism
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Survival / drug effects
  • Chemokine CCL2 / biosynthesis*
  • Cytokines / biosynthesis
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Sulfides / pharmacology*
  • Triple Negative Breast Neoplasms / genetics*
  • Triple Negative Breast Neoplasms / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Allyl Compounds
  • Biomarkers, Tumor
  • CCL2 protein, human
  • Chemokine CCL2
  • Cytokines
  • Sulfides
  • Tumor Necrosis Factor-alpha
  • diallyl trisulfide