2008
DOI: 10.1016/j.yexcr.2008.08.018
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Arachidonic acid promotes FAK activation and migration in MDA-MB-231 breast cancer cells

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Cited by 57 publications
(51 citation statements)
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“…In the profiled spectrum from negative ion mode, distinctive fatty acids and lipids were identified in breast cancer tissues. Studies indicated that mediumand long-chain free fatty acids are implicated in the activation of G protein-coupled receptors expressed in breast cancer cell lines (69)(70)(71). Some of these lipids are also known to be involved in the migration, proliferation, and invasion of breast cancer cells (i.e., oleic acid) or more generally in tumor processes (i.e., arachidonic acid) (69,(71)(72)(73)(74).…”
Section: Discussionmentioning
confidence: 99%
“…In the profiled spectrum from negative ion mode, distinctive fatty acids and lipids were identified in breast cancer tissues. Studies indicated that mediumand long-chain free fatty acids are implicated in the activation of G protein-coupled receptors expressed in breast cancer cell lines (69)(70)(71). Some of these lipids are also known to be involved in the migration, proliferation, and invasion of breast cancer cells (i.e., oleic acid) or more generally in tumor processes (i.e., arachidonic acid) (69,(71)(72)(73)(74).…”
Section: Discussionmentioning
confidence: 99%
“…However, inhibition of p38 did partially prevent PKCμ cleavage by calpain [76]. Finally, inhibition of the lipooxygenases or src prevented the increase in migration due to arachidonate [66].…”
Section: Optimizing Dietary Fatmentioning
confidence: 92%
“…Treatment of MDA-MB-231 breast cancer cells with 100-400 μM oleate promotes cell migration by approximately 2-4.7 fold. Further molecular experiments revealed this migration was induced by oleate-mediated production of arachidonate, which in turn activated focal adhesion kinase (FAK) [66]. Furthermore, 500 μM oleate induced invasion of MDA-MB-231 cells through Matrigel by approximately 2 fold [67].…”
Section: Oleatementioning
confidence: 97%
“…In NIH3T3 mouse fibroblasts, the initial transient burst in AA resulting from cPLA 2 activation is responsible for cell adhesion, with the AA metabolites leukotrienes and PGs regulating cell spreading and cell migration, respectively [93][94][95]. Other reports have shown that cPLA 2 α and its Ser-505-phosphorylated form are rapidly and specifically recruited at sites of actin polymerization such as membrane ruffles and leading edges [92].…”
Section: Cytosolic Phospholipase A2mentioning
confidence: 99%