ArticleCancers2018
Regulation of Cancer Stem Cell Metabolism by Secreted Frizzled-Related Protein 4 (sFRP4).
Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Secreted frizzled-related protein 4 (sFRP4) in cancer - Dual roles in tumorigenesis and therapeutic potential: A review.Biomolecules & biomedicine · 2025Review
- Identification of placenta-specific protein 1 (PLAC-1) expression on human PC-3 cell line-derived prostate cancer stem cells compared to the tumor parental cells.Discover oncology · 2024Article
- The role of novel adipokines in hepatocellular carcinoma progression: a mini review.American journal of cancer research · 2024Review
- Wnt Signaling and Therapeutic Resistance in Castration-Resistant Prostate Cancer.Current pharmacology reports · 2023Article
- The role of tumor microenvironment on cancer stem cell fate in solid tumors.Cell communication and signaling : CCS · 2023Review
- Sfrp4 expression in thyroxine treated calvarial cells.Life sciences · 2022Article
- Regulation of Metabolic Plasticity in Cancer Stem Cells and Implications in Cancer Therapy.Cancers · 2022Review
- SFRP4 and CDX1 Are Predictive Genes for Extragastric Recurrence of Early Gastric Cancer after Curative Resection.Journal of clinical medicine · 2022Article
- Cancer Stem Cell for Tumor Therapy.Cancers · 2021Review
- The metabolic flexibility of quiescent CSC: implications for chemotherapy resistance.Cell death & disease · 2021Review
- Tumor suppressor role of sFRP‑4 in hepatocellular carcinoma via the Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2021Article
- Epithelial Mesenchymal Transition and Progression of Breast Cancer Promoted by Diabetes Mellitus in Mice Are Associated with Increased Expression of Glycolytic and Proteolytic Enzymes.Hormones & cancer · 2020Article
- Targeting cancer stem cells from a metabolic perspective.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Studying the variations in differently expressed serum proteins of Hainan black goat during the breeding cycle using isobaric tags for relative and absolute quantitation (iTRAQ) technology.The Journal of reproduction and development · 2019Article
- Wnt Signaling in Cancer Metabolism and Immunity.Cancers · 2019Review
- PRMT1 regulates the tumour-initiating properties of esophageal squamous cell carcinoma through histone H4 arginine methylation coupled with transcriptional activation.Cell death & disease · 2019Article
- Targeting stem cells in the realm of drug-resistant breast cancer.Breast cancer (Dove Medical Press) · 2019Review
- Metabolism-Based Therapeutic Strategies Targeting Cancer Stem Cells.Frontiers in pharmacology · 2019Review
- [Expression of secreted frizzled-related protein 4 in DNA mismatch repair-deficient and mismatch repair-proficient colorectal cancers].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- The regulatory roles of lncRNAs in the process of breast cancer invasion and metastasis.Bioscience reports · 2018Review
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
Tumours contain a small number of treatment-resistant cancer stem cells (CSCs), and it is through these that tumour regrowth originates at secondary sites, thus rendering CSCs an attractive target for treatment. Cancer cells adapt cellular metabolism for aggressive proliferation. Tumour cells use less efficient glycolysis for the production of ATP and increasing tumour mass, instead of oxidative phosphorylation (OXPHOS). CSCs show distinct metabolic shift and, depending on the cancer type, can be highly glycolytic or OXPHOS dependent. Since Wnt signalling promotes glycolysis and tumour growth, we investigated the effect of the Wnt antagonist secreted frizzled-related protein 4 (sFRP4) on CSC metabolism. We demonstrate that sFRP4 has a prominent role in basal glucose uptake in CSCs derived from breast and prostate tumour cell lines. We show that sFRP4 treatment on CSCs isolated with variable glucose content induces metabolic reprogramming by relocating metabolic flux to glycolysis or OXPHOS. Altogether, sFRP4 treatment compromises cell proliferation and critically affects cell survival mechanisms such as viability, glucose transporters, pyruvate conversion, mammalian target of rapamycin, and induces CSC apoptosis under conditions of variable glucose content. Our findings provide the feasibility of using sFRP4 to inhibit CSC survival in order to induce metabolic reprogramming in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.