ArticleCancer biology & therapy2019
Inhibition of cytosolic phospholipase A2 alpha increases chemosensitivity in cervical carcinoma through suppressing β-catenin signaling.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting Cancer Stemness Using Nanotechnology in a Holistic Approach: A Narrative Review.Pharmaceutics · 2025Review
- Next generation thiazolyl ketone inhibitors of cytosolic phospholipase ANature communications · 2025Article
- Application of Nanotechnology and Phytochemicals in Anticancer Therapy.Pharmaceutics · 2024Review
- Review
- Comprehensive analysis of prognosis of cuproptosis-related oxidative stress genes in multiple myeloma.Frontiers in genetics · 2023Article
- Cancer Stem Cells and Their Possible Implications in Cervical Cancer: A Short Review.International journal of molecular sciences · 2022Review
- Logical and experimental modeling of cytokine and eicosanoid signaling in psoriatic keratinocytes.iScience · 2021Article
- Inhibition of Cytosolic Phospholipase A2α Induces Apoptosis in Multiple Myeloma Cells.Molecules (Basel, Switzerland) · 2021Article
- Targeting cPLA2α inhibits gastric cancer and augments chemotherapy efficacy via suppressing Ras/MEK/ERK and Akt/β-catenin pathways.Cancer chemotherapy and pharmacology · 2021Article
- Analytical Platforms for the Determination of Phospholipid Turnover in Breast Cancer Tissue: Role of Phospholipase Activity in Breast Cancer Development.Metabolites · 2021Review
- β-Catenin: oncogenic role and therapeutic target in cervical cancer.Biological research · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytosolic phospholipase A2alpha (cPLA2α) is a key mediator of tumorigenesis. In this study, by using a combination of pharmacological and genetic approaches in cell models and patient samples, we identify cPLA2α as a selective target to increase chemosensitivity in cervical cancer. We found that transcript and protein levels of cPLA2α but not other forms of cPLA2 (e.g., cPLA2β and cPLA2αδ) were consistently increased in all tested malignant cervical cancer cells and tissues compared to normal counterparts, suggesting that cPLA2α upregulation is a common feature in cervical cancer. We further found that promoting growth and survival rather than invasion were the predominant roles of cPLA2α on cervical cancer. In addition, chemotherapeutic agents achieved ~100% inhibition efficacy in cPLA2α-depleted cervical cancer cells, demonstrating the important role of cPLA2α in chemoresistance. Importantly, we identify that β-catenin is critically involved in the molecular mechanism of cPLA2α's action in cervical cancer. In summary, our work demonstrates the multiple essential roles of cPLA2α in cervical cancer, particularly in chemoresistance, via a β-catenin-dependent manner. Our work also suggests that targeting cPLA2α has a therapeutic value in overcoming chemoresistance in cervical cancer or other cPLA2α-regulated cancers.
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