ArticleExperimental cell research2016
Kallistatin induces breast cancer cell apoptosis and autophagy by modulating Wnt signaling and microRNA synthesis.
Article in Experimental cell research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- miRNAs as biomarkers for early cancer detection and their application in the development of new diagnostic tools.Biomedical engineering online · 2021Pooled it
- SERPINA4 facilitates colorectal cancer progression through m⁶A-dependent stabilization.Journal of translational medicine · 2026Article
- Wnt/β-Catenin-mTOR-autophagy crosstalk in breast cancer: context-dependent control of tumor progression, immune suppression, and therapeutic resistance.Frontiers in immunology · 2026Review
- Role of the Wnt signaling pathway in the complex microenvironment of breast cancer and prospects for therapeutic potential (Review).International journal of oncology · 2025Review
- The multifaceted role of kallistatin in human diseases: mechanistic insights and translational potential.Frontiers in cardiovascular medicine · 2025Review
- Mapping the function of MicroRNAs as a critical regulator of tumor-immune cell communication in breast cancer and potential treatment strategies.Frontiers in cell and developmental biology · 2024Review
- Serum proteomic profiling of precancerous gastric lesions and early gastric cancer reveals signatures associated with systemic inflammatory response and metaplastic differentiation.Frontiers in molecular biosciences · 2024Article
- Potential Therapeutic Effects of Melatonin Mediate via miRNAs in Cancer.Biochemical genetics · 2022Review
- Autophagy positively regulates Wnt signaling in mice with diabetic retinopathy.Experimental and therapeutic medicine · 2021Article
- Overexpressing microRNA-203 alleviates myocardial infarction via interacting with long non-coding RNA MIAT and mitochondrial coupling factor 6.Archives of pharmacal research · 2021Article
- Functional profiles of Müllerian inhibiting substance/anti-Müllerian hormone (MIS/AMH) in primarily cultured endometrial cancer cells.Journal of Cancer · 2021Article
- A Signature of Autophagy-Related Long Non-coding RNA to Predict the Prognosis of Breast Cancer.Frontiers in genetics · 2021Article
- TheInternational journal of women's health · 2021Article
- GPER1 and microRNA: Two Players in Breast Cancer Progression.International journal of molecular sciences · 2020Review
- Article
- The Regulatory Role of MicroRNAs in Breast Cancer.International journal of molecular sciences · 2019Review
- Neuroprotective Effects of Serpina3k in Traumatic Brain Injury.Frontiers in neurology · 2019Article
- The Long Noncoding RNA HOTAIR in Breast Cancer: Does Autophagy Play a Role?International journal of molecular sciences · 2017Review
- Kallistatin exerts anti-lymphangiogenic effects by inhibiting lymphatic endothelial cell proliferation, migration and tube formation.International journal of oncology · 2017Article
- Hypothyroidism reduces mammary tumor progression via Β-catenin-activated intrinsic apoptotic pathway in rats.Histochemistry and cell biology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Kallistatin is an endogenous protein that regulates differential signaling pathways and biological functions. Our previous studies showed that kallistatin gene therapy inhibited angiogenesis, tumor growth and metastasis in mice, and kallistatin protein suppressed Wnt-mediated growth, migration and invasion by blocking Wnt/β-catenin signaling pathway in breast cancer cells. In this study, we show that kallistatin reduced cell viability, and increased apoptotic cell death and caspase-3 activity in MDA-MB-231 breast cancer cells. Kallistatin also induced cancer cell autophagy, as evidenced by increased LC3B levels and elevated Atg5 and Beclin-1 expression; however, co-administration of Wnt or PPARγ antagonist GW9662 abolished these effects. Moreover, kallistatin via its heparin-binding site antagonized Wnt3a-induced cancer cell proliferation and increased PPARγ expression. Kallistatin inhibited oncogenic miR-21 synthesis associated with reduced Akt phosphorylation and Bcl-2 synthesis, but increased BAX expression. Kallistatin via PKC-ERK activation reduced miR-203 levels, leading to increased expression of suppressor of cytokine signaling 3 (SOCS3), a tumor suppressor. Conversely, kallistatin stimulated expression of the tumorigenic suppressors miR-34a and p53. Kallistatin's active site is essential for suppressing miR-21 and miR-203, and stimulating miR-34a and SOCS3 expression. This is the first study to demonstrate that kallistatin's heparin-binding site is essential for inhibiting Wnt-mediated effects, and its active site plays a key role in regulating miR-21, miR-203, miR-34a and SOCS3 synthesis in breast cancer cells. These findings reveal novel mechanisms of kallistatin in inducing apoptosis and autophagy in breast cancer cells, thus inhibiting tumor progression by regulation of Wnt/PPARγ signaling, as well as miR-21, miR-203 and miR-34a synthesis.
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Registered trials
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