ArticlePhysiological reports2015
Cigarette smoke induces cell motility via platelet-activating factor accumulation in breast cancer cells: a potential mechanism for metastatic disease.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- E-Cigarettes Promote Macrophage-Tumor Cells Crosstalk: Focus on Breast Carcinoma Progression and Lung Metastasis.Exploratory research and hypothesis in medicine · 2021Article
- Prolonged Exposure to Platelet Activating Factor Transforms Breast Epithelial Cells.Frontiers in genetics · 2021Article
- Zoledronic Acid Is Not Equally Potent on Osteoclasts Generated From Different Individuals.JBMR plus · 2020Article
- E-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1.Cancer letters · 2020Article
- Lipoprotein-associated phospholipase A2: The story continues.Medicinal research reviews · 2020Review
- Cigarette smoking promotes bladder cancer via increased platelet-activating factor.Physiological reports · 2019Article
- The Potential Role of Dietary Platelet-Activating Factor Inhibitors in Cancer Prevention and Treatment.Advances in nutrition (Bethesda, Md.) · 2019Review
- Inflammation, not Cholesterol, Is a Cause of Chronic Disease.Nutrients · 2018Review
- Membrane microdomains regulate NLRP10- and NLRP12-dependent signalling in A549 cells challenged with cigarette smoke extract.Archives of toxicology · 2018Article
- Platelet-inspired medicine for tumor therapy.Oncotarget · 2017Review
- Recent insights into cigarette smoking as a lifestyle risk factor for breast cancer.Breast cancer (Dove Medical Press) · 2017Review
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
- Bromoenol Lactone Attenuates Nicotine-Induced Breast Cancer Cell Proliferation and Migration.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cancer deaths are a result of metastasis rather than the primary tumor. Although cigarette smoking has been determined as a risk factor for several cancers, its role in metastasis has not been studied in detail. We propose that cigarette smoking contributes to metastatic disease via inhibition of breast cancer cell platelet-activating factor acetylhydrolase (PAF-AH), resulting in PAF accumulation and a subsequent increase in cell motility. We studied several breast cell lines, including immortalized mammary epithelial cells (MCF-10A), luminal A hormone positive MCF-7, basal-like triple negative MDA-MB-468, and claudin-low triple-negative highly metastatic MDA-MB-231 breast tumor cells. We exposed cells to cigarette smoke extract (CSE) for up to 48 h. CSE inhibited PAF-AH activity, increased PAF accumulation, and increased cell motility in MDA-MB-231 metastatic triple negative breast cancer cells. The calcium-independent phospholipase A2 (iPLA2) inhibitor, (S) bromoenol lactone ((S)-BEL) was used to prevent the accumulation of PAF and further prevented the increase in cell motility seen previously when cells were exposed to CSE. Thus, iPLA2 or PAF may represent a therapeutic target to manage metastatic disease, particularly in triple-negative breast cancer patients who smoke.
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