ArticleJournal of cellular and molecular medicine2020
PLA2G16 is a mutant p53/KLF5 transcriptional target and promotes glycolysis of pancreatic cancer.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Modeling Canine Hemangiosarcoma Progression Using Patient-Derived 2.5D Organoids and Orthotopic Xenografts.Veterinary sciences · 2026Article
- KLF5-driven TAZ-FASN signaling reprograms fatty acid metabolism to support Treg differentiation in lung cancer.Journal of translational medicine · 2026Article
- Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer.Cancer science · 2026Article
- The impact of p53 mutation on tumor immune evasion: mechanistic insights and clinical implications.Frontiers in immunology · 2026Review
- HRASLS2 promotes the growth and glycolysis of pancreatic cancer by enhancing the stability of ASPH.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- PLA2G16-Mediated Tetracosatetraenoic Acid Rewires Fatty Acid Oxidation to Impair CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A 280 bp SINE insertion within the pig PLA2G16 could potentially modify gene expression through integration with its transcript.Journal of applied genetics · 2025Article
- Multiple roles of p53 in cancer development: Regulation of tumor microenvironment, mJournal of advanced research · 2025Review
- Organoid in droplet: Production of uniform pancreatic cancer organoids from single cells.Materials today. Bio · 2025Article
- Machine Learning-Based Radiomics in Malignancy Prediction of Pancreatic Cystic Lesions: Evidence from Cyst Fluid Multi-Omics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.Journal of hematology & oncology · 2025Review
- Inhibition of KLF5 promotes ferroptosis via the ZEB1/HMOX1 axis to enhance sensitivity to oxaliplatin in cancer cells.Cell death & disease · 2025Article
- PLA2G16 expression predicts prognosis and gemcitabine sensitivity in patients with pancreatic cancer.PeerJ · 2025Article
- Abrogation of KLF5 sensitizesActa biochimica et biophysica Sinica · 2024Article
- Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer.Experimental and therapeutic medicine · 2024Article
- Genomic analysis and filtration of novel prognostic biomarkers based on metabolic and immune subtypes in pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- The Role of Krüppel-like Factors in Pancreatic Physiology and Pathophysiology.International journal of molecular sciences · 2023Review
- Cuproptosis: p53-regulated metabolic cell death?Cell death and differentiation · 2023Review
- Mechanism of NURP1 in temozolomide resistance in hypoxia-treated glioma cells via the KDM3A/TFEB axis.Oncology research · 2023Article
- The complexity of p53-mediated metabolic regulation in tumor suppression.Seminars in cancer biology · 2022Review
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
PLA2G16 is a member of the phospholipase family that catalyses the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. In the current study, we explored the functional role of PLA2G16 in pancreatic adenocarcinoma (PAAD) and the genetic/epigenetic alterations leading to its dysregulation. Bioinformatic analysis was performed using data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) and the Human Protein Atlas (HPA). Then, PANC-1 and MIA-PaCa-2 cells harbouring TP53 mutations were used for cellular and animal studies. Results showed that PL2G16 expression was significantly up-regulated in PAAD tissue and was associated with unfavourable survival. PLA2G16 inhibition suppressed pancreatic cell growth in vitro and in vivo and also inhibited aerobic glycolysis. Bioinformatic analysis indicated that KLF5 was positively correlated with PLA2G16 expression in PAAD tumours with TP53 mutation. TP53 or KLF5 inhibition significantly reduced PLA2G16 expression at both mRNA and protein levels. Dual-luciferase and chromatin Immunoprecipitation-quantitative polymerase chain reaction assays showed that KLF5 directly bound to the PLA2G16 promoter and activated its transcription. Co-immunoprecipitation assay indicated that mutant p53 had a physical interaction with KLF5. Inhibition of mutant p53 impaired the transcriptional activating effects of KLF5. In PAAD cases in TCGA, PLA2G16 expression was positively correlated with its copy number (Pearson's r = 0.51, P < 0.001), but was strongly and negatively correlated with the methylation level of cg09518969 (Pearson's r = -0.64, P < 0.001), a 5'-cytosine-phosphodiester bond-guanine-3' site within its gene locus. In conclusion, this study revealed a novel mutant p53/KLF5-PLA2G16 regulatory axis on tumour growth and glycolysis in PAAD.
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