ArticleAmerican journal of translational research2020
Fenofibrate-induced mitochondrial dysfunction and metabolic reprogramming reversal: the anti-tumor effects in gastric carcinoma cells mediated by the PPAR pathway.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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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Who cites it
32 citing papers in PubMed, 36 citations in OpenAlex.
- Redox Regulation in Glioblastoma: Mechanisms, Biomarkers, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Cannabigerol and Cannabichromene Induce Lung Cancer Cell Death and Apoptosis-Contribution of PPARα to Cannabigerol Effects.Antioxidants (Basel, Switzerland) · 2026Article
- Mechanisms of Metabolic Reprogramming Regulating Immunosuppression in the Gastric Cancer Tumor Microenvironment.Biomolecules · 2026Review
- The application of nanotechnology in regulating mitochondrial function in tumor microenvironment for cancer therapy.Theranostics · 2026Review
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Pharmacological inhibition of Peroxisome Proliferation-Activated Receptor Delta (PPARδ) imparts selective leukemia cell death.Cancer & metabolism · 2025Article
- Enhancing Mitochondrial Function Through Pharmacological Modification: A Novel Approach to Mitochondrial Transplantation in a Sepsis Model.Biomedicines · 2025Article
- Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025Review
- Drug Repurposing: A Conduit to Unravelling Metabolic Reprogramming for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Drug Repurposing for Cancer Treatment: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Article
- Systemic Reduction of Glut1 Normalizes Retinal Dysfunction, Inflammation, and Oxidative Stress in the Retina of Spontaneous Type 2 Diabetic Mice.The American journal of pathology · 2023Article
- Mitochondria Deregulations in Cancer Offer Several Potential Targets of Therapeutic Interventions.International journal of molecular sciences · 2023Review
- Peroxisome proliferator-activated receptors regulate the progression and treatment of gastrointestinal cancers.Frontiers in pharmacology · 2023Review
- Promotion of colorectal cancer cell death by ezetimibeFrontiers in pharmacology · 2023Article
- The role of cholesterol metabolism in tumor therapy, from bench to bed.Frontiers in pharmacology · 2023Review
- The role of peroxisome proliferator-activated receptors in the tumor microenvironment, tumor cell metabolism, and anticancer therapy.Frontiers in pharmacology · 2023Review
- Association between abnormal lipid metabolism and tumor.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells reprogram their metabolism to adapt to fast growth and environmental demands, which differ them from normal cells. Mitochondria are central to the malignant metabolism reprogramming process. Here, we report that PPARα was highly expressed in gastric cancer tissues and negatively correlated with prognosis. Fenofibrate, a common drug used to treat severe hypertriglyceridemia and mixed dyslipidemia, reversed cellular metabolism and mitochondrial dysfunction in gastric cancer cells through PPARα. Our results show that fenofibrate altered glucose and lipid metabolism, inhibited gastric cancer cell proliferation, and promoted apoptosis in gastric cancer cells. We further show that fenofibrate induced mitochondrial reprogramming via CPT1 and the fatty acid oxidation pathway, as well as by activating the AMPK pathway and inhibiting the HK2 pathway. Additionally, fenofibrate inhibited subcutaneous gastric cancer cell tumor growth without obvious toxicity in mice. Collectively, our results indicate that fenofibrate exhibits anti-tumor activity
Indexed as
Identifiers
32194894PMC7061836W3012686598What OpenQuestion holds
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.