Identification of potential targets for diallyl disulfide in human gastric cancer MGC-803 cells using proteomics approaches
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1Center for Gastric Cancer Research of Hunan Province, First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
Abstract:
Diallyl disulfide (DADS) is characterized as an effective agent for the prevention and therapy of cancer, however, mechanisms regarding its anticancer effects are not fully clarified. In the present study, we compared the protein expression profile of gastric cancer MGC-803 cells subjected to DADS treatment with that of untreated control cells to explore potential molecules regulated by DADS. Using proteomic approaches, we identified 23 proteins showing statistically significant differences in expression, including 9 upregulated and 14 downregulated proteins. RT-PCR and western blot analysis confirmed that retinoid-related orphan nuclear receptor α (RORα) and nM23 were increased by DADS, whereas LIM kinase-1 (LIMK1), urokinase-type plasminogen activator receptor (uPAR) and cyclin-dependent kinase-1 (CDK1) were decreased. DADS treatment and knockdown of uPAR caused suppression of ERK/Fra-1 pathway, downregulation of urokinase-type plasminogen activator (uPA), matrix metalloproteinase-9 (MMP-9) and vimentin, and upregulation of tissue inhibitor of metalloproteinase-3 (TIMP-3) and E-cadherin, concomitant with inhibition of cell migration and invasion. Moreover, knockdown of uPAR potentiated the effects of DADS on MGC-803 cells. These data demonstrate that downregulation of uPAR may partially be responsible for DADS-induced inhibition of ERK/Fra-1 pathway, as well as cell migration and invasion. Thus, the discovery of DADS-induced differential expression proteins is conducive to reveal unknown mechanisms of DADS anti-gastric cancer.
Insights
Diallyl disulfide (DADS) shows potential in gastric cancer therapy by altering protein expression. Specifically, DADS downregulates urokinase-type plasminogen activator receptor (uPAR), inhibiting cell migration and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Proteomics
Background:
- Diallyl disulfide (DADS) is recognized for its anticancer properties, but its precise mechanisms remain unclear.
- Gastric cancer remains a significant health concern, necessitating novel therapeutic strategies.
- Understanding protein expression changes induced by DADS is crucial for elucidating its anti-gastric cancer effects.
Purpose of the Study:
- To investigate the differential protein expression profile in MGC-803 gastric cancer cells treated with DADS.
- To identify key molecules regulated by DADS and explore their role in anticancer activity.
- To elucidate the molecular mechanisms underlying DADS's therapeutic potential in gastric cancer.
Main Methods:
- Proteomic analysis to compare protein expression between DADS-treated and untreated MGC-803 cells.
- RT-PCR and western blot to validate the expression levels of specific proteins.
- Gene knockdown experiments (uPAR) to assess functional consequences.
Main Results:
- Identified 23 differentially expressed proteins, with 9 upregulated and 14 downregulated.
- Confirmed upregulation of RORα and nM23, and downregulation of LIMK1, uPAR, and CDK1 by DADS.
- DADS treatment and uPAR knockdown suppressed the ERK/Fra-1 pathway, reduced invasion and migration, and altered ECM remodeling proteins.
Conclusions:
- Downregulation of uPAR is a key mechanism contributing to DADS's inhibition of cell migration and invasion.
- DADS exerts anti-gastric cancer effects partly through modulating the ERK/Fra-1 pathway and ECM-related proteins.
- The identified DADS-regulated proteins offer insights into novel therapeutic targets for gastric cancer.
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