ArticleInternational journal of molecular sciences2022
PLA2G2A Phospholipase Promotes Fatty Acid Synthesis and Energy Metabolism in Pancreatic Cancer Cells with
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- The Phospholipase AJournal of lipid and atherosclerosis · 2026Review
- Human Group IIA Secreted Phospholipase AInternational journal of molecular sciences · 2026Review
- Single-cell transcriptomic insights into lipoprotein transport in yolk sac membrane endodermal epithelial cells of chicken embryos.Poultry science · 2026Article
- Mitochondrial Abundant Heat Soluble (MAHS) Protein Expression Modulates Metabolic Dynamics in Human Adipose-Derived Stem Cells.International journal of molecular sciences · 2026Article
- Review
- Metabolic Salvage and Acyl-chain Remodeling Support Glycosphingolipid Synthesis within the PDAC Tumor Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Combining spatial and single-cell transcriptome data to analyze tertiary lymphoid structures in clear cell renal cell carcinoma reveals prognostic biomarkers.Journal of translational medicine · 2026Article
- The value of lipid metabolism-related genes in pancreatic cancer immunotherapy and drug prediction.Journal of gastrointestinal oncology · 2025Article
- Multi-omics analysis unveils the role of cancer-associated fibroblasts in cutaneous squamous cell carcinoma.Cancer cell international · 2025Article
- Drugging the 'undruggable' KRAS: breakthroughs, challenges, and opportunities in pancreatic cancer.Cancer biology & medicine · 2025Review
- Cardiolipin Dysregulation in Glioblastoma-Effects on Mitochondrial Function Tumor Cell Death and Sensitivity to Mitochondria-Targeting Drugs.Journal of cellular physiology · 2025Review
- Targeting lipid metabolism: novel insights and therapeutic advances in pancreatic cancer treatment.Lipids in health and disease · 2025Review
- Targeting KRAS: from metabolic regulation to cancer treatment.Molecular cancer · 2025Review
- Article
- Identification of arachidonic acid metabolism-related diagnostic markers in heart failure based on bioinformatics analysis and machine learning.Frontiers in cardiovascular medicine · 2025Article
- Transcriptional insights into gastrointestinal adaptations in pigs to high altitude.Frontiers in veterinary science · 2025Article
- Blockade of glucose-6-phosphate dehydrogenase induces immunogenic cell death and accelerates immunotherapy.Journal for immunotherapy of cancer · 2024Article
- Single-cell transcriptomics analysis of bullous pemphigoid unveils immune-stromal crosstalk in type 2 inflammatory disease.Nature communications · 2024Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenic K-ras is often activated in pancreatic ductal adenocarcinoma (PDAC) due to frequent mutation (>90%), which drives multiple cellular processes, including alterations in lipid metabolism associated with a malignant phenotype. However, the role and mechanism of the altered lipid metabolism in K-ras-driven cancer remains poorly understood. In this study, using human pancreatic epithelial cells harboring inducible K-rasG12D (HPNE/K-rasG12D) and pancreatic cancer cell lines, we found that the expression of phospholipase A2 group IIA (PLA2G2A) was upregulated by oncogenic K-ras. The elevated expression of PLA2G2A was also observed in pancreatic cancer tissues and was correlated with poor survival of PDAC patients. Abrogation of PLA2G2A by siRNA or by pharmacological inhibition using tanshinone I significantly increased lipid peroxidation, reduced fatty acid synthase (FASN) expression, and impaired mitochondrial function manifested by a decrease in mitochondrial transmembrane potential and a reduction in ATP production, leading to the inhibition of cancer cell proliferation. Our study suggests that high expression of PLA2G2A induced by oncogenic K-ras promotes cancer cell survival, likely by reducing lipid peroxidation through its ability to facilitate the removal of polyunsaturated fatty acids from lipid membranes by enhancing the de novo fatty acid synthesis and energy metabolism to support cancer cell proliferation. As such, PLA2G2A might function as a downstream mediator of K-ras and could be a potential therapeutic target.
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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.