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Diallyl Trisulfide Suppresses the Renal Cancer Stem-like Cell Properties via Nanog
Taotao Zhang1,2, Wanshuang Cao3, Hongliang Sun4
1Health Management Center , The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Abstract:
Cancer stem-like cells (CSCs), which play an important role in tumor initiation and progression, have been identified in many cancers. Diallyl trisulfide (DATS) is an organosulfur compound extracted from garlic with anticancer activities. Nanog is a transcription factor responsible for maintaining the stemness of CSCs, but its role in the DATS-induced attenuation of renal CSC properties is unknown. In this study, renal CSCs were enriched from human renal cancer cell lines 786-O and ACHN cultured in a serum-free medium (SFM). The properties of CSCs were analyzed by evaluating the ability of the cells in sphere formation and measuring the expression of stem cell markers. We found that downregulation of Nanog inhibited renal CSC properties. DATS suppressed renal CSC activities by reducing tumorsphere formation, decreasing stem cell markers including Nanog, CD44, ALDH1A1, and Oct4, inhibiting cell proliferation and promoting apoptosis. We further revealed that overexpression of Nanog reversed the suppressive effects of DATS on renal CSCs. Taken together, our results demonstrated that DATS inhibited renal CSCs by suppressing Nanog. These novel findings suggested that, through Nanog targeting, DATS can potentially be used as an anti-tumor agent for renal cancer.
Insights
Diallyl trisulfide (DATS) inhibits renal cancer stem cell properties by suppressing Nanog. This suggests DATS may be a potential anti-tumor agent for renal cancer by targeting Nanog.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Stem Cell Research
Background:
- Cancer stem-like cells (CSCs) drive tumor initiation and progression in various cancers.
- Diallyl trisulfide (DATS), a garlic-derived compound, exhibits anticancer properties.
- The role of Nanog in DATS's effect on renal CSCs remains unclear.
Purpose of the Study:
- To investigate the effect of DATS on renal CSCs and its underlying mechanism involving Nanog.
- To determine if Nanog is a key mediator in DATS-induced suppression of renal CSC properties.
Main Methods:
- Enrichment of renal CSCs from human renal cancer cell lines (786-O and ACHN) in serum-free medium.
- Assessment of CSC properties via tumorsphere formation assays and stem cell marker expression (Nanog, CD44, ALDH1A1, Oct4).
- Evaluation of DATS treatment effects and Nanog overexpression on renal CSC activity, proliferation, and apoptosis.
Main Results:
- Downregulation of Nanog diminished renal CSC properties.
- DATS suppressed renal CSCs by reducing tumorsphere formation, decreasing stem cell markers, inhibiting proliferation, and promoting apoptosis.
- Overexpression of Nanog counteracted the suppressive effects of DATS on renal CSCs.
Conclusions:
- DATS effectively inhibits renal CSCs, with Nanog suppression being a key mechanism.
- Targeting Nanog with DATS shows potential as a therapeutic strategy for renal cancer treatment.
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