FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3037263465> ?p ?o ?g. }

• W3037263465 abstract "Pancreatic cancer is an aggressive disease characterized by invasiveness, rapid progression and profound resistance to treatment. It is the fourth leading cause of cancer mortality with a 5-year survival rate of only 6%. Accumulating evidence indicates that sphingolipids play critical roles in cancer growth and dissemination. In particular, ceramide 1- phosphate (C1P), which is formed by the action of ceramide kinase on ceramide, stimulates cell proliferation (1), and promotes cell survival (2, 3). The mechanisms by which C1P stimulates cell growth involves activation of extracellularly regulated kinases 1 and 2 (ERK1/2), phosphatidylinositol 3-kinase (PI3K), c-Jun N-terminal kinase (JNK), or mammalian target of rapamycin (mTOR), whereas C1P-enhanced cell survival implicates inhibition of serine palmitoyl transferase (SPT) and acid sphingomylinase (ASMase) (4). More recently, we found that C1P enhances human pancreatic cancer cell migration and invasion potently and that this effect is completely abolished by pertussis toxin (PTX), suggesting the participation of a Gi protein-coupled receptor in this process. We also observed that human pancreatic cancer cells migrate spontaneously. However, contrary to the effect of C1P, spontaneous cell migration was insensitive to treatment with PTX (5). Investigation into the mechanisms responsible for spontaneous migration of the pancreatic cancer cells revealed that ceramide kinase (CerK) is a key enzyme in the regulation of this process. In fact, inhibition of CerK activity, or treatment with specific CerK siRNA to silence the gene encoding this kinase, potently reduced migration of the pancreatic cancer cells. By contrast, overexpression of CerK stimulated cell migration, an action that was concomitant with prolonged phosphorylation of ERK1-2 and Akt, in a PTX independent manner. It can be concluded that the axis CerK/C1P plays a critical role in pancreatic cancer cell migration/invasion, and that targeting CerK expression or activity may be a relevant factor for controlling pancreatic cancer cell dissemination.Ceramide 1-phosphate (C1P) is bioactive sphingolipid metabolite first shown to regulate cell growth and death of the cell. The subsequent studies revealed to C1P was a potent stimulator of cytosolic phospholipase A2 (cPLA2) with ensuing release the arachidonic acid and prostaglandin biosynthesis. The latter findings placed C1P on the list of pro-inflammatory metabolites. As more recently C1P was found to potently stimulate cell migration an action that is associated to diverse physiological effects and as well as to inflammatory responses following with tumor dissemination. The implication of C1P in inflammation has gained further interest in last few years due to the discovery it can exert anti-inflammatory actions in some of the cell types and tissues. In particular, C1P has been demonstrated to inhibit pro-inflammatory cytokine release & blockade of pro-inflammatory transcription factor NF-κB in some cell types, as to reduce airway inflammation and lung emphysema. The present review is focused on novel aspects of the C1P regulation of cell migration and impact of C1P as novel anti-inflammatory agent. Gloss: Ceramide 1-phosphate (C1P) is phosphosphingolipid with potent biological activities. It promotes cell growth and survival and is a key regulator of cell migration. Both C1P and the enzyme that catalyzes its biosynthesis, ceramide kinase are implicated in inflammatory responses. Although C1P has pro-inflammatory properties it reduces pulmonary emphysema and exerts anti-inflammatory actions in the lung. Synthetic C1P analogs may be promising tools to treat lung inflammation.Keywords: Pancreatic cancer, sphingolipids, ceramide kinase, ceramide-1-phosphateNote: This work is partly presented at 29th Euro-Global Summit on Cancer Therapy & Radiation Oncology on July 23-25, 2018 held at Rome, Italy." @default.
• W3037263465 created "2020-07-02" @default.
• W3037263465 creator A5049646572 @default.
• W3037263465 date "2020-01-01" @default.
• W3037263465 modified "2023-09-23" @default.
• W3037263465 title "Euro Cancer 2018: Regulation of pancreatic cancer cell migration by the axis ceramide kinase/ceramide 1-phosphate - Antonio Gomez-Munoz - University of the Basque Country" @default.
• W3037263465 hasPublicationYear "2020" @default.
• W3037263465 type Work @default.
• W3037263465 sameAs 3037263465 @default.
• W3037263465 citedByCount "0" @default.
• W3037263465 crossrefType "journal-article" @default.
• W3037263465 hasAuthorship W3037263465A5049646572 @default.
• W3037263465 hasConcept C104202773 @default.
• W3037263465 hasConcept C121608353 @default.
• W3037263465 hasConcept C137738243 @default.
• W3037263465 hasConcept C1491633281 @default.
• W3037263465 hasConcept C184235292 @default.
• W3037263465 hasConcept C190283241 @default.
• W3037263465 hasConcept C2777851122 @default.
• W3037263465 hasConcept C2780210213 @default.
• W3037263465 hasConcept C502942594 @default.
• W3037263465 hasConcept C54355233 @default.
• W3037263465 hasConcept C55493867 @default.
• W3037263465 hasConcept C62112901 @default.
• W3037263465 hasConcept C62478195 @default.
• W3037263465 hasConcept C86554907 @default.
• W3037263465 hasConcept C86803240 @default.
• W3037263465 hasConcept C95444343 @default.
• W3037263465 hasConcept C96232424 @default.
• W3037263465 hasConceptScore W3037263465C104202773 @default.
• W3037263465 hasConceptScore W3037263465C121608353 @default.
• W3037263465 hasConceptScore W3037263465C137738243 @default.
• W3037263465 hasConceptScore W3037263465C1491633281 @default.
• W3037263465 hasConceptScore W3037263465C184235292 @default.
• W3037263465 hasConceptScore W3037263465C190283241 @default.
• W3037263465 hasConceptScore W3037263465C2777851122 @default.
• W3037263465 hasConceptScore W3037263465C2780210213 @default.
• W3037263465 hasConceptScore W3037263465C502942594 @default.
• W3037263465 hasConceptScore W3037263465C54355233 @default.
• W3037263465 hasConceptScore W3037263465C55493867 @default.
• W3037263465 hasConceptScore W3037263465C62112901 @default.
• W3037263465 hasConceptScore W3037263465C62478195 @default.
• W3037263465 hasConceptScore W3037263465C86554907 @default.
• W3037263465 hasConceptScore W3037263465C86803240 @default.
• W3037263465 hasConceptScore W3037263465C95444343 @default.
• W3037263465 hasConceptScore W3037263465C96232424 @default.
• W3037263465 hasIssue "2" @default.
• W3037263465 hasLocation W30372634651 @default.
• W3037263465 hasOpenAccess W3037263465 @default.
• W3037263465 hasPrimaryLocation W30372634651 @default.
• W3037263465 hasRelatedWork W1265317767 @default.
• W3037263465 hasRelatedWork W1966245642 @default.
• W3037263465 hasRelatedWork W1983727064 @default.
• W3037263465 hasRelatedWork W1998691880 @default.
• W3037263465 hasRelatedWork W2019200307 @default.
• W3037263465 hasRelatedWork W2019491412 @default.
• W3037263465 hasRelatedWork W2027429767 @default.
• W3037263465 hasRelatedWork W2033424069 @default.
• W3037263465 hasRelatedWork W2039337809 @default.
• W3037263465 hasRelatedWork W2039692456 @default.
• W3037263465 hasRelatedWork W2083995751 @default.
• W3037263465 hasRelatedWork W2109688906 @default.
• W3037263465 hasRelatedWork W2182085413 @default.
• W3037263465 hasRelatedWork W2314120999 @default.
• W3037263465 hasRelatedWork W2562175277 @default.
• W3037263465 hasRelatedWork W2779206441 @default.
• W3037263465 hasRelatedWork W2798153493 @default.
• W3037263465 hasRelatedWork W2921128088 @default.
• W3037263465 hasRelatedWork W292267549 @default.
• W3037263465 hasRelatedWork W3201455056 @default.
• W3037263465 hasVolume "5" @default.
• W3037263465 isParatext "false" @default.
• W3037263465 isRetracted "false" @default.
• W3037263465 magId "3037263465" @default.
• W3037263465 workType "article" @default.