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Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast
Konan J W Kanga1, Patricia Mendonca1, Karam F A Soliman1
1Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A.
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.
Insights
Diallyl trisulfide (DATS) shows promise in treating triple-negative breast cancer (TNBC). It effectively reduced cancer cell death and migration, potentially by targeting CCL2 signaling pathways.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Diallyl trisulfide (DATS) exhibits chemopreventive properties against breast cancer.
- CCL2/MCP-1 is implicated in breast cancer progression.
- Triple-negative breast cancer (TNBC) remains a challenging subtype to treat.
Purpose of the Study:
- To investigate the efficacy of DATS on TNBC cells.
- To explore the impact of DATS on key signaling pathways in TNBC.
- To assess the role of CCL2/MCP-1 in DATS-mediated effects on TNBC.
Main Methods:
- Treatment of TNF-α-induced TNBC cells with DATS.
- Cell viability assessed using trypan blue exclusion.
- Cell migration evaluated via wound-healing assays.
- Cytokine expression analyzed using human cytokine arrays, ELISA, and RT-PCR.
Main Results:
- DATS significantly induced cell death and inhibited cell migration in TNBC cells.
- DATS decreased CCL2/MCP-1 expression in MDA-MB-231 cells, but not MDA-MB-468 cells.
- DATS down-regulated mRNA expression of IKBKE and MAPK8, suggesting involvement of NF-κB and MAPK signaling.
Conclusions:
- DATS demonstrates therapeutic potential for TNBC.
- Targeting CCL2 may be a mechanism by which DATS exerts its effects.
- DATS warrants further investigation for TNBC prevention and treatment strategies.
