ArticleCancer chemotherapy and pharmacology2021
Targeting cPLA2α inhibits gastric cancer and augments chemotherapy efficacy via suppressing Ras/MEK/ERK and Akt/β-catenin pathways.
Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- cPLA2α inhibition potentiates anti-PD-1 immunotherapy in lung adenocarcinoma via remodeling tumor microenvironment.Communications biology · 2026Article
- Pirin Transcriptionally Regulates PLA2G4A To Inhibit Ferroptosis in Colorectal Cancer via Lipid Profile Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PI3K Signaling at the Crossroads of Lipid Metabolism and Cancer.Advances in experimental medicine and biology · 2025Review
- Exploring the mechanism of Synechococcus sp. XM-24 in gastric cancer treatment via network pharmacology and molecular docking.PloS one · 2025Article
- PLA2G4A and ACHE modulate lipid profiles via glycerophospholipid metabolism in platinum-resistant gastric cancer.Journal of translational medicine · 2024Article
- Emetine, a small molecule natural product, displays potent anti-gastric cancer activity via regulation of multiple signaling pathways.Cancer chemotherapy and pharmacology · 2023Article
- Association of plasma lipid metabolism profiles with overall survival for patients with gastric cancer undergoing gastrectomy based onNutrition & metabolism · 2023Article
- Association between abnormal lipid metabolism and tumor.Frontiers in endocrinology · 2023Review
- The Role of Lipid Metabolism in Gastric Cancer.Frontiers in oncology · 2022Review
- Natural product manoalide promotes EGFR-TKI sensitivity of lung cancer cells by KRAS-ERK pathway and mitochondrial CaFrontiers in pharmacology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCytosolic phospholipase A2alpha (cPLA2α), an enzyme that is responsible for the hydrolysis of membrane phospholipids, is a key mediator of tumor transformation, progression and metastasis. The role of cPLA2α in gastric cancer has not been revealed.
methodscPLA2α expression was analyzed using RT-PCR and immunohistochemistry approaches in gastric cancer patient samples (n = 26) and multiple cell lines (n = 7). cPLA2α function was studied using plasmid overexpression and siRNA knockdown approaches in SNU-1, MKN-74 and MKN-45 cell lines. The downstream effectors of cPLA2α were determined using biochemical assays.
resultscPLA2α upregulation is a common feature in gastric cancer patients, particularly those with metastasis. cPLA2α overexpression is sufficient to promote gastric cancer cell growth and migration, and confer chemo-resistance. cPLA2α depletion is active against gastric cancer via inhibiting growth and migration, and inducing apoptosis in gastric cancer cells. Of note, cPLA2α depletion augments efficacy of chemotherapy. Mechanistic studies confirm that cPLA2α regulates gastric cancer biological activities via mainly regulating Ras/MEK/ERK and possibly Akt/β-catenin pathways. Pearson correlation coefficient analysis also suggests a moderate positive correlation between cPLA2α and RAS in gastric cancer.
conclusionsOur work demonstrates cPLA2α inhibition as a therapeutic strategy to overcome chemo-resistance and highlights the association of cPLA2α and Ras in gastric cancer.
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