ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Hydroxysafflor-Yellow A Induces Human Gastric Carcinoma BGC-823 Cell Apoptosis by Activating Peroxisome Proliferator-Activated Receptor Gamma (PPARγ).
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- C2H2 Zinc-Finger Transcription Factors Coordinate Hormone-Stress Crosstalk to Shape Expression Bias of the Flavonoid Pathway in Safflower (Current issues in molecular biology · 2025Article
- Pharmacological actions and applications of safflower flavonoids.Frontiers in nutrition · 2025Review
- PPARG Activation of Fatty Acid Metabolism Drives Resistance to Anti-HER2 Therapies in HER2-Positive Breast Cancer.International journal of biological sciences · 2025Article
- Hydroxysafflor yellow A: a natural pigment with potential anticancer therapeutic effect.Frontiers in pharmacology · 2024Review
- The role of peroxisome proliferator-activated receptors in the tumor microenvironment, tumor cell metabolism, and anticancer therapy.Frontiers in pharmacology · 2023Review
- Hydroxysafflor yellow A inhibits the proliferation, migration, and invasion of colorectal cancer cells through the PPARγ/PTEN/Akt signaling pathway.Bioengineered · 2021Article
- Potential of Bioactive Food Components against Gastric Cancer: Insights into Molecular Mechanism and Therapeutic Targets.Cancers · 2021Review
- PPAR-γ Modulators as Current and Potential Cancer Treatments.Frontiers in oncology · 2021Review
- Hydroxysafflor yellow A induces autophagy in human liver cancer cells by regulating Beclin 1 and ERK expression.Experimental and therapeutic medicine · 2020Article
- Therapeutic potential of PPARγ natural agonists in liver diseases.Journal of cellular and molecular medicine · 2020Review
- Antioxidant and Pro-Oxidant Properties of Carthamus Tinctorius, Hydroxy Safflor Yellow A, and Safflor Yellow A.Antioxidants (Basel, Switzerland) · 2020Article
- NDRG1 was downregulated and worked as favorable biomarker in the development of gastric cancer.Translational cancer research · 2020Article
- Three Ingredients of Safflower Alleviate Acute Lung Injury and Inhibit NET Release Induced by Lipopolysaccharide.Mediators of inflammation · 2020Article
- MicroRNA-150-5p and SRC kinase signaling inhibitor 1 involvement in the pathological development of gastric cancer.Experimental and therapeutic medicine · 2019Article
- Hydroxysafflor yellow A inhibited lipopolysaccharide-induced non-small cell lung cancer cell proliferation, migration, and invasion by suppressing the PI3K/AKT/mTOR and ERK/MAPK signaling pathways.Thoracic cancer · 2019Article
- Hydroxysafflor Yellow A: A Promising Therapeutic Agent for a Broad Spectrum of Diseases.Evidence-based complementary and alternative medicine : eCAM · 2018Review
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Authors and funding
13 authors.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Anti-tumor properties of hydroxysafflor-yellow A (HSYA) have been recently revealed, as a series of apoptotic factors were confirmed to be regulated by HSYA and associated with peroxisome proliferator-activated receptor Gamma (PPARγ). In this study, we investigated the cell apoptosis mechanism of HSYA via activated PPARγ signal in human gastric carcinoma cells. MATERIAL AND METHODS BGC-823 cells were cultured and divided into 5 independent groups: Tumor, HSYA, HSYA+PPARγ inhibitor (GW9662), and PPARg agonist (RGZ), RGZ+GW9662. Cell proliferative activity was measured by MTT. Apoptosis and cell cycle were detected by flow cytometry. The nuclear translocation of PPARγ was detected by immunofluorescence staining chemistry, and mRNA levels of PPARγ and caspase-3 were measured by real-time qPCR. RESULTS Compared to the RGZ group, the HSYA group (100 µM) showed a similar inhibitory effect on the proliferation process of BGC-823 cells, inducing their apoptosis. As a result, the transition of BGC-823 cells from G0/G1 phase to S phase was blocked. HSYA was also found to promote the nuclear translocation of PPARγ, leading to increased expression of PPARγ and caspase-3. The regulatory effect of HSYA on BGC-823 cells could be further inhibited by PPARγ inhibitor in group GW9662. CONCLUSIONS We report the inhibitory effect of HSYA on the proliferation of BGC-823 cells, which results in activating PPARg-dependent cell cycle blocking and cell apoptosis, suggesting that PPARg is a specific type of HSYA that can induce apoptosis of BGC-823 cells.
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