Enhanced breast cancer cell adherence to the lung endothelium via PAF acetylhydrolase inhibition: a potential mechanism for enhanced metastasis in smokers

Kispert, Shannon; Marentette, John; McHowat, Jane

doi:10.1152/ajpcell.00218.2014

Cited by 25 publications

(33 citation statements)

References 28 publications

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“…CSE treatment also resulted in increased PAF and PAF receptor (PAF-R) expression 15. CSE-treated MDA-MB-231 cells were added to human lung microvascular endothelial cells (HMVEC-L) exhibited increased cell adherence when compared with untreated cells 46. The increased cell adherence could be abrogated by pretreatment with (S)-bromoenol lactone ((S)-BEL, an iPLA 2 β inhibitor) and Ginkgolide B, a PAF-R antagonist 46.…”

Section: Breast Cancer and Smoking: Evidence For A Direct Linkmentioning

confidence: 99%

Recent insights into cigarette smoking as a lifestyle risk factor for breast cancer

Kispert¹,

McHowat²

2017

BCTT

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There have been many cohort studies published reviewing the epidemiological evidence that links breast cancer to cigarette smoking, yet the underlying mechanisms are largely unknown and research studies are few and incomplete. Although cohort studies are important in establishing a connection between breast cancer and cigarette smoking, basic science research is necessary to prove the relationship and to highlight potential interventions and drug targets that can be used to manage the disease. This subject has been controversial for many decades; however, there has been a recent resurgence in interest because of the widespread acknowledgment of the role lifestyle choices play in cancer development and progression. This review will detail the current statistics associated with cigarette smoking and discuss recent cohort and basic research studies that highlight the association of cigarette smoking and breast cancer initiation and progression.

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Section: Breast Cancer and Smoking: Evidence For A Direct Linkmentioning

confidence: 99%

Recent insights into cigarette smoking as a lifestyle risk factor for breast cancer

Kispert¹,

McHowat²

2017

BCTT

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“…Normal mammary epithelial cell line MCF‐10A exhibited no PAF‐R expression even after 48 h of CSE exposure (Kispert et al. ).…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke induces cell motility via platelet-activating factor accumulation in breast cancer cells: a potential mechanism for metastatic disease

2015

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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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“…Cigarette smoke is considered as one of the factors which result in the accumulation of PAF by inhibiting PAF-AH [13,14] . This accumulated PAF enhances adherence of metastatic breast cancer cells to lung endothelium [15] .…”

Section: Research Highlightmentioning

confidence: 99%

Platelet activating factor leads to initiation and promotion of breast cancer

Anandi

Lahiri

2016

Cancer Cell Microenviron

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Bioactive molecules present in the tumor milieu are known to contribute substantially to tumor progression. Phospholipid mediators are a group of molecules that have roles in normal physiology as well as in pathological conditions. Platelet activating factor (PAF), a phospholipd mediator, secreted by cells present in tumor microenvironment has been implicated to have a possible role in cancer progression. Here, we highlight our study of the potential role of PAF in inducing transformation of breast epithelial cells grown as three dimensional cultures. We have also attempted to dissect the motility related molecular pathway activated upon PAF stimulation in MDA-MB 231 cells. This study further calls for detailed analysis of pathways downstream of PAF signalling which would aid in identification of targets and designing of treatment strategies.

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Enhanced breast cancer cell adherence to the lung endothelium via PAF acetylhydrolase inhibition: a potential mechanism for enhanced metastasis in smokers

Cited by 25 publications

References 28 publications

Recent insights into cigarette smoking as a lifestyle risk factor for breast cancer

Recent insights into cigarette smoking as a lifestyle risk factor for breast cancer

Cigarette smoke induces cell motility via platelet-activating factor accumulation in breast cancer cells: a potential mechanism for metastatic disease

Platelet activating factor leads to initiation and promotion of breast cancer

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