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PI3K is required for both basal and LPA-induced DNA synthesis in oral carcinoma cells.
Aasrum, Monica; Tjomsland, Vegard; Thoresen, G Hege; De Angelis, Paula M; Christoffersen, Thoralf; Brusevold, Ingvild J.
Afiliación
  • Aasrum M; Department of Pharmacology, Institute of Clinical Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway.
  • Tjomsland V; Department of Pharmacology, Institute of Clinical Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway.
  • Thoresen GH; Department of Hepato-Pancreato-Biliary Surgery, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
  • De Angelis PM; Department of Pharmacology, Institute of Clinical Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway.
  • Christoffersen T; Department of Pharmaceutical Biosciences, School of Pharmacy, University of Oslo, Oslo, Norway.
  • Brusevold IJ; Clinic for Diagnostics and Intervention, Department of Pathology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
J Oral Pathol Med ; 45(6): 425-32, 2016 Jul.
Article en En | MEDLINE | ID: mdl-26602326
BACKGROUND: The glycerophospholipid lysophosphatidic acid (LPA), which is present in most tissues and in high concentrations in saliva, may exert profound effects on oral cancer cells. We have investigated mitogenic signalling induced by LPA in the two oral carcinoma cell lines, D2 and E10, focusing on the role of EGFR transactivation and downstream pathways. METHODS: Two oral squamous carcinoma cell lines, D2 and E10, were analysed for effects of LPA on signalling pathways and induction of DNA synthesis. Pathway activation was investigated by examining phosphorylation of signalling proteins and by the use of specific pathway inhibitors. RESULTS: The D2 cells had higher levels of activated signalling proteins and higher DNA synthesis activity in the basal condition than E10 cells. EGF did not induce proliferation in D2 cells, whereas LPA induced proliferation in both cell lines, by mechanisms depending on EGFR transactivation. Release of EGFR ligands was involved in basal and LPA-induced proliferation in both D2 and E10 cells. The proliferation in D2 cells was dependent on the PI3K/Akt pathway, but not the MEK/ERK pathway. In E10 cells, the PI3K/Akt, MEK/ERK and p38 pathways were all involved in the proliferation. CONCLUSION: Transactivation of EGFR is required for LPA-induced DNA synthesis in D2 and E10 cells. Our results also show that although proliferation of oral carcinoma cells is regulated by several pathways, and differentially in E10 and D2 cells, the PI3K pathway has a crucial role in both cell lines.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ADN de Neoplasias / Neoplasias de la Boca / Lisofosfolípidos / Carcinoma de Células Escamosas / Fosfatidilinositol 3-Quinasas / Neoplasias de Cabeza y Cuello Límite: Humans Idioma: En Revista: J Oral Pathol Med Asunto de la revista: ODONTOLOGIA / PATOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Noruega Pais de publicación: Dinamarca
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ADN de Neoplasias / Neoplasias de la Boca / Lisofosfolípidos / Carcinoma de Células Escamosas / Fosfatidilinositol 3-Quinasas / Neoplasias de Cabeza y Cuello Límite: Humans Idioma: En Revista: J Oral Pathol Med Asunto de la revista: ODONTOLOGIA / PATOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Noruega Pais de publicación: Dinamarca