ArticleCell death & disease2017
cPLA2α mediates TGF-β-induced epithelial-mesenchymal transition in breast cancer through PI3k/Akt signaling.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 68 citations in OpenAlex.
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- cPLA2α inhibition potentiates anti-PD-1 immunotherapy in lung adenocarcinoma via remodeling tumor microenvironment.Communications biology · 2026Article
- Spatiotemporally programmed nanomedicine engineering to resolve conflicting immunosignals in triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- Tumor Lipidomic Changes after Treatment with Polymeric Hydroxychloroquine in a Syngeneic Murine Model of Pancreatic Cancer.ACS omega · 2026Article
- Novel Perspective for Prognostic Stratification and Personalized Therapy in Breast Cancer Patients: Development of Cancer Stem Cells and Metabolism-Associated Prognostic Model.International journal of women's health · 2026Article
- Decoding the mechanisms underlying breast cancer brain metastasis: paving the way for precision therapeutics.Biomarker research · 2025Review
- A prognostic model for multiple myeloma based on lipid metabolism related genes.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- ZMYND8 drives HER2 antibody resistance in breast cancer via lipid control of IL-27.Nature communications · 2025Article
- Pinostilbene inhibits lung epithelial-mesenchymal transition and delays pulmonary fibrosis by modulating the PI3K/Akt pathway.Frontiers in pharmacology · 2025Article
- Dual roles of innate immune cells and cytokines in shaping the breast cancer microenvironment.Frontiers in immunology · 2025Review
- PSAT1 mediated EMT of colorectal cancer cells by regulating Pl3K/AKT signaling pathway.Journal of Cancer · 2024Article
- Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Volume-regulated anion channels conduct ATP in undifferentiated mammary cells and promote tumorigenesis in xenograft nude mouse.Frontiers in cell and developmental biology · 2024Article
- The Phospholipase A2 Superfamily: Structure, Isozymes, Catalysis, Physiologic and Pathologic Roles.International journal of molecular sciences · 2023Review
- Comprehensive analysis of prognosis of cuproptosis-related oxidative stress genes in multiple myeloma.Frontiers in genetics · 2023Article
- Lipids in cancer: a global view of the contribution of lipid pathways to metastatic formation and treatment resistance.Oncogenesis · 2022Review
- cPLA2 blockade attenuates S100A7-mediated breast tumorigenicity by inhibiting the immunosuppressive tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2022Article
- The impact of decreased expression of SVEP1 on abnormal neovascularization and poor prognosis in patients with intrahepatic cholangiocarcinoma.Frontiers in genetics · 2022Article
- Low expression and Hypermethylation of ATP2B1 in Intrahepatic Cholangiocarcinoma Correlated With Cold Tumor Microenvironment.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A high incidence of tumor recurrence and metastasis has been reported in breast cancer patients; nevertheless, the underlying molecular mechanisms are largely unknown. Epithelial-mesenchymal transition (EMT), which is induced by transforming growth factor-β (TGF-β), has been implicated in tumorigenesis and breast cancer metastasis. EMT events are now directly associated with tumor metastasis, and this progress is dependent on the inflammatory microenvironment. Cytosolic phospholipase A2α (cPLA2α) has been shown to participate in a series of biological processes including inflammation and cancer development. However, the role and molecular mechanism of cPLA2α in breast cancer EMT and metastasis remain enigmatic. In this study, we found that cPLA2α was commonly overexpressed in most human breast cancer tissues and significantly correlated with a poor prognosis for human breast cancer. Functional studies demonstrated that cPLA2α overexpression was significantly associated with elevated migration and invasion in MDA-MB-231 and T47D cells. Conversely, reduced cPLA2α expression strongly attenuated metastasis and the EMT program of MDA-MB-231 cells. Further study found that knockdown of cPLA2α in MDA-MB-231 cells inhibited TGF-β-induced EMT through the PI3K/Akt signaling pathway. Animal experiments revealed that cPLA2α downregulation in MDA-MB-231 cells markedly restrained tumorigenesis and metastasis in vivo. This study indicates the potential role of cPLA2α in breast cancer metastasis and indicates that this molecule is a promising therapeutic target for breast cancer.
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