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The Suppressing Effects of Dkk3 Expression on Aggressiveness and Tumorigenesis of Colorectal Cancer
Shuang Zhao1, Chang-Lai Hao2, En-Hong Zhao3
1Department of Oncology and Experimental Center, The Affiliated Hospital of Chengde Medical University, Chengde, China.
Abstract:
Dkk3 has been discovered during comparison of immortalized and parental cells. Its expression has been shown to reduce colony formation and induce apoptosis of cancer cells, acting as a tumor suppressor. Herein, we demonstrate that Dkk3 overexpression or protein treatment may inhibit colorectal cancer cell proliferation, migration, and invasion and that they may promote apoptosis and G2 phase arrest with hypoexpression of Bcl-2, cdc25B, cdc25c, N-cadherin, slug, and twist and hyperexpression of Bax and E-cadherin. This effect is consistent with that of recombinant Dkk3 exposure and blocked with anti-Dkk3 antibody. Dkk3 deletion in intestinal cells was not associated with the emergence of epithelial lesions; however, adenoma emerged after sodium desoxycholate treatment. At both mRNA and protein levels, Dkk3 expression was higher in normal than in cancer tissues (p<0.05). Dkk3 mRNA expression was negatively associated with its promoter methylation, growth pattern, differentiation, and favorable prognosis in the patients with colorectal cancer (p<0.05). Dkk3-related signal pathways in colorectal cancer included those of cellular adhesion and migration, melanogenesis, chemokine, Hedgehog, JAK-STAT, TOLL-like receptor, TGF-β, MAPK, and calcium signaling (p<0.05). These findings indicate that Dkk3 expression levels can help assess cancer aggressiveness and patient prognosis. It might also suppress aggressive phenotypes and tumorigenesis as a molecular target in gene therapy.
Insights
Dickkopf-3 (Dkk3) acts as a tumor suppressor, inhibiting colorectal cancer progression. Dkk3 overexpression reduces cancer cell proliferation and invasion, offering a potential therapeutic target for colorectal cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Dickkopf-3 (Dkk3) is recognized for its tumor-suppressive properties, including reducing colony formation and inducing apoptosis in cancer cells.
- Previous studies suggest Dkk3's role in cancer, but its specific mechanisms and therapeutic potential in colorectal cancer require further elucidation.
Purpose of the Study:
- To investigate the effects of Dkk3 overexpression and protein treatment on colorectal cancer cell behavior.
- To analyze the association between Dkk3 expression levels and colorectal cancer aggressiveness, prognosis, and related signaling pathways.
Main Methods:
- Assessing the impact of Dkk3 on colorectal cancer cell proliferation, migration, invasion, apoptosis, and cell cycle progression.
- Analyzing Dkk3 expression in normal and cancerous colorectal tissues at both mRNA and protein levels.
- Correlating Dkk3 mRNA expression with promoter methylation, tumor differentiation, and patient prognosis.
- Examining Dkk3-associated signaling pathways in colorectal cancer.
Main Results:
- Dkk3 overexpression or protein treatment inhibited colorectal cancer cell proliferation, migration, and invasion, while promoting apoptosis and G2 phase arrest.
- Dkk3 expression was significantly higher in normal tissues compared to cancer tissues.
- Lower Dkk3 mRNA expression correlated with promoter methylation, aggressive growth patterns, poor differentiation, and unfavorable prognosis in colorectal cancer patients.
- Dkk3-related signaling pathways involved cellular adhesion, migration, and various cancer-associated signaling cascades.
Conclusions:
- Dkk3 exhibits significant tumor-suppressive activity against colorectal cancer by inhibiting aggressive phenotypes.
- Dkk3 expression levels serve as a valuable biomarker for assessing colorectal cancer aggressiveness and patient prognosis.
- Dkk3 represents a promising molecular target for gene therapy in colorectal cancer treatment.
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