ArticlePloS one2011
Lysophosphatidate induces chemo-resistance by releasing breast cancer cells from taxol-induced mitotic arrest.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- Inhibition of autotaxin activity with IOA-289 decreases fibrosis in mouse E0771 breast tumors.International journal of cancer · 2025Article
- Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Article
- Targeting lysophosphatidic acid receptor with Ki16425 impedes T cell lymphoma progression through apoptosis induction, glycolysis inhibition, and activation of antitumor immune response.Apoptosis : an international journal on programmed cell death · 2022Article
- Influence of the autotaxin-lysophosphatidic acid axis on cellular function and cytokine expression in different breast cancer cell lines.Scientific reports · 2022Article
- Review
- Lipid Phosphate Phosphatases and Cancer.Biomolecules · 2020Review
- The Importance of Breast Adipose Tissue in Breast Cancer.International journal of molecular sciences · 2020Review
- Regulation of tumor cell - Microenvironment interaction by the autotaxin-lysophosphatidic acid receptor axis.Advances in biological regulation · 2019Review
- Lysophosphatidic acid enhances breast cancer cells-mediated osteoclastogenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- MAPT (Tau) expression is a biomarker for an increased rate of survival in pediatric neuroblastoma.Cell cycle (Georgetown, Tex.) · 2018Article
- Recent advances in targeting the autotaxin-lysophosphatidate-lipid phosphate phosphatase axis in vivo.Journal of biomedical research · 2016Review
- Co-treatment by docetaxel and vinblastine breaks down P-glycoprotein mediated chemo-resistance.Iranian journal of basic medical sciences · 2016Article
- The role of Six1 signaling in paclitaxel-dependent apoptosis in MCF-7 cell line.Bosnian journal of basic medical sciences · 2016Article
- Autotaxin, a lysophospholipase D with pleomorphic effects in oncogenesis and cancer progression.Journal of lipid research · 2016Review
- Lipid phosphate phosphatases and their roles in mammalian physiology and pathology.Journal of lipid research · 2015Review
- Aberrant expression and potential therapeutic target of lysophosphatidic acid receptor 3 in triple-negative breast cancers.Clinical and experimental medicine · 2015Article
- Meaningful prevention of breast cancer metastasis: candidate therapeutics, preclinical validation, and clinical trial concerns.Journal of molecular medicine (Berlin, Germany) · 2015Review
- Lipid phosphate phosphatase-1 expression in cancer cells attenuates tumor growth and metastasis in mice.Journal of lipid research · 2014Article
- Bioactive lipids, LPC and LPA, are novel prometastatic factors and their tissue levels increase in response to radio/chemotherapy.Molecular cancer research : MCR · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTaxol is a microtubule stabilizing agent that arrests cells in mitosis leading to cell death. Taxol is widely used to treat breast cancer, but resistance occurs in 25-69% of patients and it is vital to understand how Taxol resistance develops to improve chemotherapy. The effects of chemotherapeutic agents are overcome by survival signals that cancer cells receive. We focused our studies on autotaxin, which is a secreted protein that increases tumor growth, aggressiveness, angiogenesis and metastasis. We discovered that autotaxin strongly antagonizes the Taxol-induced killing of breast cancer and melanoma cells by converting the abundant extra-cellular lipid, lysophosphatidylcholine, into lysophosphatidate. This lipid stimulates specific G-protein coupled receptors that activate survival signals. METHODOLOGY/PRINCIPAL
findingsIn this study we determined the basis of these antagonistic actions of lysophosphatidate towards Taxol-induced G2/M arrest and cell death using cultured breast cancer cells. Lysophosphatidate does not antagonize Taxol action in MCF-7 cells by increasing Taxol metabolism or its expulsion through multi-drug resistance transporters. Lysophosphatidate does not lower the percentage of cells accumulating in G2/M by decreasing exit from S-phase or selective stimulation of cell death in G2/M. Instead, LPA had an unexpected and remarkable action in enabling MCF-7 and MDA-MB-468 cells, which had been arrested in G2/M by Taxol, to normalize spindle structure and divide, thus avoiding cell death. This action involves displacement of Taxol from the tubulin polymer fraction, which based on inhibitor studies, depends on activation of LPA receptors and phosphatidylinositol 3-kinase. CONCLUSIONS/SIGNIFICANCE: This work demonstrates a previously unknown consequence of lysophosphatidate action that explains why autotaxin and lysophosphatidate protect against Taxol-induced cell death and promote resistance to the action of this important therapeutic agent.
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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.