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


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 07 09 2021
revised: 28 09 2021
accepted: 04 10 2021
entrez: 1 12 2021
pubmed: 2 12 2021
medline: 15 12 2021
Statut: ppublish

Résumé

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

Sections du résumé

BACKGROUND/AIM OBJECTIVE
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 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 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 CONCLUSIONS
DATS may have a role in TNBC therapy and prevention by targeting CCL2.

Identifiants

pubmed: 34848446
pii: 41/12/5919
doi: 10.21873/anticanres.15411
pmc: PMC8691120
mid: NIHMS1762576
doi:

Substances chimiques

Allyl Compounds 0
Biomarkers, Tumor 0
CCL2 protein, human 0
Chemokine CCL2 0
Cytokines 0
Sulfides 0
Tumor Necrosis Factor-alpha 0
diallyl trisulfide 0ZO1U5A3XX

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

5919-5933

Subventions

Organisme : NIMHD NIH HHS
ID : P20 MD006738
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007582
Pays : United States

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

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Auteurs

Konan J W Kanga (KJW)

Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A.

Patricia Mendonca (P)

Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A.

Karam F A Soliman (KFA)

Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A.

Dominique T Ferguson (DT)

Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A.

Selina F Darling-Reed (SF)

Division of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, U.S.A. selina.darling@famu.edu sdarlingreed@gmail.com.

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Classifications MeSH