ArticleActa pharmacologica Sinica2010
Downregulation of Dickkopf-1 is responsible for high proliferation of breast cancer cells via losing control of Wnt/beta-catenin signaling.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Wnt signaling in cancer: from biomarkers to targeted therapies and clinical translation.Molecular cancer · 2025Review
- Modulation of Wnt/Beta-Catenin Pathway by Major Dietary Phytochemicals Against Breast Cancer Development.Biology · 2025Review
- Correlation of NNMT and DKK1 Protein Expression With Clinicopathological Characteristics and Prognosis of Breast Cancer.Clinical Medicine Insights. Oncology · 2023Article
- The role of epigenetic modifications in drug resistance and treatment of breast cancer.Cellular & molecular biology letters · 2022Review
- Investigation of the Antitumor Effects of Tamoxifen and Its Ferrocene-Linked Derivatives on Pancreatic and Breast Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Canine osteosarcoma in comparative oncology: Molecular mechanisms through to treatment discovery.Frontiers in veterinary science · 2022Review
- Herbal Ingredients in the Prevention of Breast Cancer: Comprehensive Review of Potential Molecular Targets and Role of Natural Products.Oxidative medicine and cellular longevity · 2022Review
- Article
- The Clinical Diagnostic and Prognostic Value of Dickkopf-1 in Cancer.Cancer management and research · 2020Review
- MicroRNA-216a suppresses the proliferation and migration of human breast cancer cells via the Wnt/β-catenin signaling pathway.Oncology reports · 2019Article
- EBV miR-BART10-3p Promotes Cell Proliferation and Migration by Targeting DKK1.International journal of biological sciences · 2019Article
- Dickkopf-1 (Dkk1) protein expression in breast cancer with special reference to bone metastases.Clinical & experimental metastasis · 2018Article
- Breast cancer development and progression: Risk factors, cancer stem cells, signaling pathways, genomics, and molecular pathogenesis.Genes & diseases · 2018Review
- The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling.Acta pharmacologica Sinica · 2018Article
- Breast cancer lung metastasis: Molecular biology and therapeutic implications.Cancer biology & therapy · 2018Review
- The role of Dickkopf family in cancers: from Bench to Bedside.American journal of cancer research · 2017Review
- The best of both worlds - managing the cancer, saving the bone.Nature reviews. Endocrinology · 2016Review
- The Wnt inhibitor dickkopf-1: a link between breast cancer and bone metastases.Clinical & experimental metastasis · 2015Review
- PDGF beta targeting in cervical cancer cells suggest a fine-tuning of compensatory signalling pathways to sustain tumourigenic stimulation.Journal of cellular and molecular medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the role of DKK-1/Wnt/beta-catenin signaling in high proliferation of LM-MCF-7 breast cancer cells, a sub-clone of MCF-7 cell line.
methodsTwo cell lines (MCF-7 and LM-MCF-7) with different proliferation abilities were used. LM-MCF-7 cells were transiently transfected with the pcDNA3-DKK-1 plasmid encoding the DKK-1 gene (or MCF-7 cells were transfected siRNA targeting DKK-1 mRNA). Flow cytometry analysis and 5-bromo-2'-deoxyuridine (BrdU) incorporation assay were applied to detect the cell proliferation. The expression levels of beta-catenin, phosphorylated beta-catenin, c-Myc, cyclin D1 and Survivin were examined by Western blot analysis. The regulation of Survivin was investigated by Luciferase reporter gene assay.
resultsWestern blot and RT-PCR analysis showed that the expression level of DKK-1 was downregulated in LM-MCF-7 relative to MCF-7 cells. Flow cytometry and BrdU incorporation assay showed DKK-1 could suppress growth of breast cancer cells. Overexpression of DKK-1 was able to accelerate phosphorylation-dependent degradation of beta-catenin and downregulate the expression of beta-catenin, c-Myc, cyclin D1 and Survivin. Luciferase reporter gene assay demonstrated that Survivin could be regulated by beta-catenin/TCF4 pathway.
conclusionWe conclude that the downregulation of DKK-1 is responsible for the high proliferation ability of LM-MCF-7 breast cancer cells via losing control of Wnt/beta-catenin signaling pathway, in which c-Myc, cyclinD1 and Survivin serve as essential downstream effectors. Our finding provides a new insight into the mechanism of breast cancer cell proliferation.
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