Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells
| Autor: | Selina Darling-Reed, Patricia Mendonca, Dominique T. Ferguson, Konan J W Kanga, Karam F.A. Soliman |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
Programmed cell death Cell Survival medicine.medical_treatment Apoptosis Triple Negative Breast Neoplasms Sulfides CCL2 Article chemistry.chemical_compound Cell Movement Cell Line Tumor Biomarkers Tumor medicine Humans IKBKE Chemokine CCL2 Triple-negative breast cancer Tumor Necrosis Factor-alpha Chemistry General Medicine Allyl Compounds Gene Expression Regulation Neoplastic Cytokine Diallyl trisulfide Oncology Cell culture Cancer research Cytokines Female Tumor necrosis factor alpha |
| Zdroj: | Anticancer Res |
| ISSN: | 1791-7530 0250-7005 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|