title: Inhibition of LN-308 glioma cell proliferation and migration by retinoic acid amide through activation of Akt pathway.
abstract: The present study was performed to investigate the effect of retinoic acid amide (RAA) on the expression of integrin α3β1, rate of cell proliferation and migration in p53-deficient glioma cell line, LN-308. The results revealed promotion of integrin α3 expression, reduction in proliferation and migration in RAA treated cells compared to the control LN-308 glioma cells. Promotion of RAA induced integrin α3β1 expression led to the enhancement in cyclin-dependent kinase nuclear localization and activation of Akt pathway. In addition, RAA treatment inhibited the expression of nuclear factor-κB, Bcl-2 and epidermal growth factor receptor (EGFR). These factors are responsible for promoting the rate of cell proliferation and survival in the carcinoma cells. Thus RAA treatment inhibits rate of LN-308 glioma cell proliferation and migration through increase in integrin α3β1 expression and activation of Akt pathway. Therefore, RAA can be of therapeutic importance for the treatment of glioma.
authors.affiliation: Department of Neurosurgery, Brain Hospital, Affiliated Hospital of Qingdao UniversityQingdao, China; Department of Neurosurgery, People's Hospital of Laiwu CityLaiwu, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Neurosurgery, People's Hospital of Laiwu City Laiwu, China.
authors.forename: Xiang-Dong
authors.initials: XD
authors.lastname: Lu
authors.affiliation: Department of Neurosurgery, People's Hospital of Laiwu City Laiwu, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Si
authors.affiliation: Department of Neurosurgery, People's Hospital of Laiwu City Laiwu, China.
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Song
authors.affiliation: Department of Neurosurgery, Brain Hospital, Affiliated Hospital of Qingdao University Qingdao, China.
authors.forename: Qing-Hai
authors.initials: QH
authors.lastname: Meng
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D001932:Brain Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018797:Cell Cycle Proteins / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D004789:Enzyme Activation; D066246:ErbB Receptors / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D039201:Integrin alpha3beta1 / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009361:Neoplasm Invasiveness; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D034622:RNA Interference; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014162:Transfection; D014212:Tretinoin / Q000031:analogs & derivatives* / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; C000595707:BCL2 protein, human; D018797:Cell Cycle Proteins; D039201:Integrin alpha3beta1; D016328:NF-kappa B; D047428:Protein Kinase Inhibitors; D019253:Proto-Oncogene Proteins c-bcl-2; D014212:Tretinoin; C054441:retinamide; C512478:EGFR protein, human; D066246:ErbB Receptors; D051057:Proto-Oncogene Proteins c-akt
keywords: Retinoic acid amide; glioma; localization; migration; proliferation
references.citation: Cancer Res. 1998 Dec 1;58(23):5537-45
references.pmid: 9850091
references.citation: Blood. 1999 Feb 1;93(3):1045-61
references.pmid: 9920855
references.citation: Prostate. 1999 Feb 15;38(3):228-36
references.pmid: 10068347
references.citation: Carcinogenesis. 1999 Feb;20(2):255-60
references.pmid: 10069462
references.citation: Int J Cancer. 1999 Mar 15;80(6):935-43
references.pmid: 10074929
references.citation: Trends Mol Med. 2005 Mar;11(3):97-103
references.pmid: 15760767
references.citation: Nat Rev Cancer. 2005 May;5(5):341-54
references.pmid: 15864276
references.citation: J Neurooncol. 1997 Sep;34(2):145-51
references.pmid: 9210061
references.citation: J Neurooncol. 1997 Sep;34(2):169-77
references.pmid: 9210065
references.citation: Oncogene. 1997 Oct 23;15(17):2037-48
references.pmid: 9366521
references.citation: J Clin Oncol. 1998 Mar;16(3):1060-7
references.pmid: 9508191
references.citation: Eur J Cancer. 1998 Jan;34(1):111-7
references.pmid: 9624247
references.citation: Cutis. 1998 Feb;61(2 Suppl):40-5
references.pmid: 9787993
references.citation: Clin Cancer Res. 1996 Dec;2(12):1931-5
references.pmid: 9816151
references.citation: Cell Death Differ. 2006 Dec;13(12):2033-41
references.pmid: 16628233
references.citation: Nat Rev Cancer. 2007 Mar;7(3):169-81
references.pmid: 17318210
references.citation: Expert Rev Mol Med. 2010;12:e3
references.pmid: 20078909
references.citation: Cell. 2010 Jun 25;141(7):1117-34
references.pmid: 20602996
references.citation: Nat Rev Drug Discov. 2010 Oct;9(10):804-20
references.pmid: 20885411
references.citation: Nat Rev Cancer. 2012 Feb;12(2):121-32
references.pmid: 22257950
references.citation: Cancer Res. 2000 Jul 15;60(14):3689-95
references.pmid: 10919634
references.citation: Curr Opin Cell Biol. 2000 Oct;12(5):548-53
references.pmid: 10978888
references.citation: Cell. 2002 Sep 20;110(6):673-87
references.pmid: 12297042
references.citation: Nat Rev Cancer. 2002 Feb;2(2):91-100
references.pmid: 12635172
references.citation: J Biol Chem. 2003 May 23;278(21):18980-9
references.pmid: 12649266
references.citation: Cancer Sci. 2004 Feb;95(2):142-8
references.pmid: 14965364
references.citation: Exp Oncol. 2004 Jun;26(2):106-10
references.pmid: 15273661