title: Requirement of Osteopontin in the migration and protection against Taxol-induced apoptosis via the ATX-LPA axis in SGC7901 cells.
abstract: BACKGROUND
  Autotaxin (ATX) possesses lysophospholipase D (lyso PLD) activity, which converts lysophosphatidylcholine (LPC) into lysophosphatidic acid (LPA). The ATX-LPA signaling axis has been implicated in angiogenesis, chronic inflammation and tumor progression. Osteopontin (OPN) is an important chemokine involved in the survival, proliferation, migration, invasion and metastasis of gastric cancer cells. The focus of the present study was to investigate the relationship between the ATX-LPA axis and OPN.
  
  
  RESULTS
  In comparison with non-treated cells, we found that the ATX-LPA axis up-regulated OPN expression by 1.92-fold in protein levels and 1.3-fold in mRNA levels. The ATX-LPA axis activates LPA2, Akt, ERK and ELK-1 and also protects SGC7901 cells from apoptosis induced by Taxol treatment.
  
  
  CONCLUSIONS
  This study provides the first evidence that expression of OPN induced by ATX-LPA axis is mediated by the activation of Akt and MAPK/ERK pathways through the LPA2 receptor. In addition, OPN is required for the protective effects of ATX-LPA against Taxol-induced apoptosis and ATX-LPA-induced migration of SGC7901 cells.
authors.affiliation: Department of Gastroenterology, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Rihua
authors.initials: R
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Shijie
authors.initials: S
authors.lastname: Ma
authors.forename: Zuhu
authors.initials: Z
authors.lastname: Huang
authors.forename: Guoxin
authors.initials: G
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008246:Lysophospholipids / Q000378:metabolism; D009097:Multienzyme Complexes / Q000235:genetics / Q000378:metabolism*; D053495:Osteopontin / Q000235:genetics / Q000378:metabolism*; D017239:Paclitaxel / Q000494:pharmacology; D043264:Phosphodiesterase I / Q000235:genetics / Q000378:metabolism*; D010727:Phosphoric Diester Hydrolases; D017027:Protein Tyrosine Phosphatases / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D011755:Pyrophosphatases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D049368:Receptors, Lysophosphatidic Acid / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation; D050807:ets-Domain Protein Elk-1 / Q000235:genetics / Q000378:metabolism; D000099189:Lysophospholipase D
chemical_list: D008246:Lysophospholipids; D009097:Multienzyme Complexes; D053495:Osteopontin; D017239:Paclitaxel; D043264:Phosphodiesterase I; D010727:Phosphoric Diester Hydrolases; D017027:Protein Tyrosine Phosphatases; D051057:Proto-Oncogene Proteins c-akt; D011755:Pyrophosphatases; D012333:RNA, Messenger; D049368:Receptors, Lysophosphatidic Acid; D050807:ets-Domain Protein Elk-1; D000099189:Lysophospholipase D; C494112:ELK1 protein, human; C096335:B59 protein, human; C032881:lysophosphatidic acid