ArticleDigestive diseases and sciences2013
Lysophosphatidic acid stimulates activation of focal adhesion kinase and paxillin and promotes cell motility, via LPA1-3, in human pancreatic cancer.
Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Impact of tumor necrosis factor-alpha and lysophosphatidic acid on the behavior of ovarian cancer cells in a three-dimensional collagen hydrogel.The journal of obstetrics and gynaecology research · 2025Article
- Is Lipid Metabolism of Value in Cancer Research and Treatment? Part I- Lipid Metabolism in Cancer.Metabolites · 2024Review
- The Role of Paxillin Aberrant Expression in Cancer and Its Potential as a Target for Cancer Therapy.International journal of molecular sciences · 2023Review
- Review
- ATX/LPA axis regulates FAK activation, cell proliferation, apoptosis, and motility in human pancreatic cancer cells.In vitro cellular & developmental biology. Animal · 2022Article
- Lysophosphatidic Acid Signaling and microRNAs: New Roles in Various Cancers.Frontiers in oncology · 2022Review
- Review
- The LPAInternational journal of molecular sciences · 2021Review
- Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target.Frontiers in cell and developmental biology · 2021Review
- GPCRs in pancreatic adenocarcinoma: Contributors to tumour biology and novel therapeutic targets.British journal of pharmacology · 2020Review
- Review
- ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Focal Adhesion Kinase Expression in Ameloblastoma: A Preliminary Observational Study.Journal of clinical and diagnostic research : JCDR · 2017Article
- Autotaxin-Lysophosphatidic Acid: From Inflammation to Cancer Development.Mediators of inflammation · 2017Review
- Article
- Advances in Lipidomics for Cancer Biomarkers Discovery.International journal of molecular sciences · 2016Review
- Bit1 knockdown contributes to growth suppression as well as the decreases of migration and invasion abilities in esophageal squamous cell carcinoma via suppressing FAK-paxillin pathway.Molecular cancer · 2016Article
- Fenretinide Perturbs Focal Adhesion Kinase in Premalignant and Malignant Human Oral Keratinocytes. Fenretinide's Chemopreventive Mechanisms Include ECM Interactions.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer cells.Familial cancer · 2015Article
- Promising pharmacological directions in the world of lysophosphatidic Acid signaling.Biomolecules & therapeutics · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic cancer is highly metastatic and with poor prognosis. In previous studies, lysophosphatidic acid (LPA) was shown to be a critical component of ascites which promoted the invasion and metastasis of pancreatic cancer. Two focal adhesion proteins, focal adhesion kinase (FAK) and paxillin, were crucially involved in cell migration, cytoskeleton reorganization, and the dynamics of focal adhesion.
objectivesThis study examined the involvement of LPA1-3 in LPA-induced activation of FAK and paxillin, and in cell motility, in pancreatic cancer PANC-1 cells.
methodsReverse transcriptase polymerase chain reaction analysis was used to examine mRNA expression of LPA receptors in PANC-1. Cellular protein expression of FAK and paxillin was analyzed by western blotting. The subcellular location of FAK and paxillin was visualized by immunofluorescence. Cell migration was measured by use of a transwell migration chamber.
resultsThree LPA receptors (LPA1, LPA2, and LPA3) were significantly expressed in PANC-1 cells. Treatment with LPA induced both time and dose-dependent tyrosine phosphorylation of FAK and paxillin. LPA also affected translocation of FAK and paxillin from cytoplasm to focal adhesions at the cell periphery and enhanced cell motility of PANC-1. Pretreatment with 3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl)benzylsulfanyl)propanoic acid (Ki16425), an antagonist of LPA1 and LPA3, before LPA attenuated the LPA-induced tyrosine phosphorylation and redistribution of FAK and paxillin and abrogated LPA-induced cellular migration activity.
conclusionsThese results suggest LPA induces activation of FAK and paxillin via LPA1-3, which may contribute to the increased cell motility in human pancreatic cancer PANC-1 cells. Thus, an understanding of the regulation by LPA of cell motility in pancreatic cancer could identify novel targets for therapy.
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