ArticleOxidative medicine and cellular longevity2019
Betulinic Acid Suppresses Breast Cancer Metastasis by Targeting GRP78-Mediated Glycolysis and ER Stress Apoptotic Pathway.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 106 citations in OpenAlex.
- Pentacyclic Triterpenoid Acids in the Treatment of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- The Inclusion of Dietary and Medicinal Mushrooms into Translational Oncology: Pros and Cons at the Molecular Level.International journal of molecular sciences · 2026Review
- Targeting phosphofructokinase in cancer: integrating natural products for metabolic reprogramming and therapeutic innovation.Frontiers in pharmacology · 2026Review
- Advances and challenges in betulinic acid therapeutics and delivery systems for breast cancer prevention and treatment.RSC advances · 2025Review
- Emerging phytochemical-based nanocarriers: redefining the perspectives of breast cancer therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Plant-derived terpenoids modulating cancer cell metabolism and cross-linked signaling pathways: an updated reviews.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Role of Plant-Derived Natural Products as a Regulator of the Tyrosine Kinase Pathway in the Management of Lung Cancer.Current issues in molecular biology · 2025Review
- Comprehensive characterization of respiratory genes based on a computational framework in pan-cancer to develop stratified treatment strategies.PLoS computational biology · 2025Article
- Advances in the structures, mechanisms and targeting of molecular chaperones.Signal transduction and targeted therapy · 2025Review
- Modulating the tumor microenvironment: The role of traditional Chinese medicine in improving lung cancer treatment.Open life sciences · 2025Review
- AEGAN-Pathifier: a data augmentation method to improve cancer classification for imbalanced gene expression data.BMC bioinformatics · 2024Article
- Unveiling the pharmacological potential of plant triterpenoids in breast cancer management: an updated review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Endoplasmic reticulum stress-a key guardian in cancer.Cell death discovery · 2024Review
- Combination of betulinic acid and EGFR-TKIs exerts synergistic anti-tumor effects against wild-type EGFR NSCLC by inducing autophagy-related cell death via EGFR signaling pathway.Respiratory research · 2024Article
- Betulinic Acid for Glioblastoma Treatment: Reality, Challenges and Perspectives.International journal of molecular sciences · 2024Review
- The therapeutic effect of traditional Chinese medicine on breast cancer through modulation of the Wnt/β-catenin signaling pathway.Frontiers in pharmacology · 2024Review
- Immunologic Crosstalk of Endoplasmic Reticulum Stress Signaling in Bladder Cancer.Current cancer drug targets · 2024Review
- The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies.International journal of molecular sciences · 2023Review
- Dihydroartemisinin inhibits liver cancer cell migration and invasion by reducing ATP synthase production through CaMKK2/NCLX.Oncology letters · 2023Article
- Phytochemicals Target Multiple Metabolic Pathways in Cancer.Antioxidants (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting aberrant metabolism is a promising strategy for inhibiting cancer growth and metastasis. Research is now geared towards investigating the inhibition of glycolysis for anticancer drug development. Betulinic acid (BA) has demonstrated potent anticancer activities in multiple malignancies. However, its regulatory effects on glycolysis and the underlying molecular mechanisms are still unclear. BA inhibited invasion and migration of highly aggressive breast cancer cells. Moreover, BA could suppress aerobic glycolysis of breast cancer cells presenting as a reduction of lactate production, quiescent energy phenotype transition, and downregulation of aerobic glycolysis-related proteins. In this study, glucose-regulated protein 78 (GRP78) was also identified as the molecular target of BA in inhibiting aerobic glycolysis. BA treatment led to GRP78 overexpression, and GRP78 knockdown abrogated the inhibitory effect of BA on glycolysis. Further studies demonstrated that overexpressed GRP78 activated the endoplasmic reticulum (ER) stress sensor PERK. Subsequent phosphorylation of eIF2
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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.