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Cited by 57Wnt/β-catenin signaling in development and cancerPI3K/AKT/mTOR signaling in cancerGlioma Diagnosis and Treatment

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Inactivation of PI3K/AKT signaling inhibits glioma cell growth through modulation of β-catenin-mediated transcription

Han, Lei, Yang, Yang, Yue, Xiao, Huang, Kai, Liu, Xiaomin, Pu, Peiyu, Jiang, Hao, Yan, Wei, Jiang, Tao, Kang, Chunsheng·2010·Brain Research
DOI 10.1016/j.brainres.2010.09.097
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Abstract

Aberrant Wnt/β-catenin signaling contributes to the development of many cancers, including glial tumorigenesis. While cross talk between the Wnt/β-catenin and PI3K/AKT signaling pathways has been proposed, the impact of PI3K/AKT inhibition on β-catenin signaling in glioma remains unknown. In the present study, we report decreased cell proliferation and invasive ability upon the LY294002-induced inhibition of PI3K in both U251 and LN229 human glioblastoma cells in vitro. Pharmacologic inhibition of PI3K resulted in the downregulation of several members of the β-catenin pathway, including Fra-1, c-Myc, and cyclin D1. Downregulation impacted β-catenin-mediated transcription, as LY294002 decreased β-catenin/TCF transcriptional activity, determined by the reporter assay. Similar results were observed in vivo, as intratumoral injection of LY294002 downregulated the expression of the components of the β-catenin pathway and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts. These results suggest that the PI3K/AKT signaling pathway regulates glioma cell proliferation, in part via repression of the Wnt/β-catenin pathway.

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Research works printed but not linked: 37

  1. Baryawno, 2010, Small-molecule inhibitors of phosphatidylinositol 3-kinase/Akt signaling inhibit Wnt/beta-catenin pathway cross-talk and suppress medulloblastoma growth, Cancer Res., 1, 266, 10.1158/0008-5472.CAN-09-0578 · DOI
  2. Brantley, 2008, Signal transducer and activator of transcription-3: a molecular hub for signaling pathways in gliomas, Mol. Cancer Res., 5, 675, 10.1158/1541-7786.MCR-07-2180 · DOI
  3. Clements, 2003, Adenomatous polyposis coli/beta-catenin interaction and downstream targets: altered gene expression in gastrointestinal tumors, Clin. Colorectal Cancer, 2, 113, 10.3816/CCC.2003.n.018 · DOI
  4. Cohen, 1988, fra-1: a serum-inducible, cellular immediate-early gene that encodes a Fos-related antigen, Mol. Cell. Biol., 5, 2063, 10.1128/MCB.8.5.2063 · DOI
  5. Cohen, 1989, The product of a fos-related gene, fra-1, binds cooperatively to the AP-1 site with Jun: transcription factor AP-1 is comprised of multiple protein complexes, Genes Dev., 2, 173, 10.1101/gad.3.2.173 · DOI
  6. Cully, 2006, Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis, Nat. Rev. Cancer, 3, 184, 10.1038/nrc1819 · DOI
  7. Datta, 1999, Cellular survival: a play in three Akts, Genes Dev., 22, 2905, 10.1101/gad.13.22.2905 · DOI · Paper page
  8. Debinski, 2005, Fos-related antigen 1 modulates malignant features of glioma cells, Mol. Cancer Res., 4, 237, 10.1158/1541-7786.MCR-05-0004 · DOI
  9. Fang, 2007, Phosphorylation of beta-catenin by AKT promotes beta-catenin transcriptional activity, J. Biol. Chem., 15, 11221, 10.1074/jbc.M611871200 · DOI
  10. Fu, 2009, Inhibitory effects of adenovirus mediated Akt1 and PIK3R1 shRNA on the growth of malignant tumor cells in vitro and in vivo, Cancer Biol. Ther., 11, 1002, 10.4161/cbt.8.11.8285 · DOI
  11. Furnari, 2007, Malignant astrocytic glioma: genetics, biology, and paths to treatment, Genes Dev., 21, 2683, 10.1101/gad.1596707 · DOI · Paper page
  12. Han, 2010, Tat–BMPs–PAMAM conjugates enhance therapeutic effect of small interference RNA on U251 glioma cells in vitro and in vivo, Hum. Gene Ther., 4, 417, 10.1089/hum.2009.087 · DOI
  13. Hosack, 2003, Identifying biological themes within lists of genes with EASE, Genome Biol., 10, R70, 10.1186/gb-2003-4-10-r70 · DOI
  14. Jean, 2009, Epidermal growth factor receptor/beta-catenin/T-cell factor 4/matrix metalloproteinase 1: a new pathway for regulating keratinocyte invasiveness after UVA irradiation, Cancer Res., 8, 3291, 10.1158/0008-5472.CAN-08-1909 · DOI
  15. Kang, 2006, Suppression of EGFR expression by antisense or small interference RNA inhibits U251 glioma cell growth in vitro and in vivo, Cancer Gene Ther., 5, 530, 10.1038/sj.cgt.7700932 · DOI
  16. Karim, 2004, The significance of the Wnt pathway in the pathology of human cancers, Pathology, 2, 120, 10.1080/00313020410001671957 · DOI
  17. Korinek, 1997, Constitutive transcriptional activation by a beta-catenin–Tcf complex in APC−/− colon carcinoma, Science, 5307, 1784, 10.1126/science.275.5307.1784 · DOI · Paper page
  18. Kotliarova, 2008, Glycogen synthase kinase-3 inhibition induces glioma cell death through c-MYC, nuclear factor-kappaB, and glucose regulation, Cancer Res., 16, 6643, 10.1158/0008-5472.CAN-08-0850 · DOI
  19. Lee, 2005, Membrane depolarization induces the undulating phosphorylation/dephosphorylation of glycogen synthase kinase 3beta, and this dephosphorylation involves protein phosphatases 2A and 2B in SH-SY5Y human neuroblastoma cells, J. Biol. Chem., 23, 22044, 10.1074/jbc.M413987200 · DOI
  20. Liu, X., Wang, L., Zhao, S., Ji. X., Luo, Y., Ling, F., 2010. beta-Catenin overexpression in malignant glioma and its role in proliferation and apoptosis in glioblastma cells. (DOI: 10.1007/s12032-010-9476-5). · DOI
  21. Louis, 2007, The 2007 WHO classification of tumours of the central nervous system, Acta Neuropathol. (Berl), 2, 97, 10.1007/s00401-007-0243-4 · DOI
  22. Lu, 2003, Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion, Cancer Cell, 6, 499, 10.1016/S1535-6108(03)00304-0 · DOI
  23. Mann, 1999, Target genes of beta-catenin–T cell-factor/lymphoid-enhancer- factor signaling in human colorectal carcinomas, Proc. Natl Acad. Sci. USA, 4, 1603, 10.1073/pnas.96.4.1603 · DOI · Paper page
  24. Mendelsohn, 2000, The EGF receptor family as targets for cancer therapy, Oncogene, 56, 6550, 10.1038/sj.onc.1204082 · DOI
  25. Mikels, 2006, Wnts as ligands: processing, secretion and reception, Oncogene, 57, 7461, 10.1038/sj.onc.1210053 · DOI
  26. Morali, 2001, IGF-II induces rapid beta-catenin relocation to the nucleus during epithelium to mesenchyme transition, Oncogene, 36, 4942, 10.1038/sj.onc.1204660 · DOI
  27. Nikuseva, 2010, Changes of AXIN-1 and beta-catenin in neuroepithelial brain tumors, Pathol. Oncol. Res., 1, 75, 10.1007/s12253-009-9190-9 · DOI
  28. Ohgaki, 2007, Genetic pathways to primary and secondary glioblastoma, Am. J. Pathol., 5, 1445, 10.2353/ajpath.2007.070011 · DOI
  29. Pu, 2004, Antisense and dominant-negative AKT2 cDNA inhibits glioma cell invasion, Tumour Biol., 4, 172, 10.1159/000081099 · DOI
  30. Pu, 2006, Downregulation of PIK3CB by siRNA suppresses malignant glioma cell growth in vitro and in vivo, Technol. Cancer Res. Treat., 3, 271, 10.1177/153303460600500308 · DOI
  31. Pu, 2006, The effects of antisense AKT2 RNA on the inhibition of malignant glioma cell growth in vitro and in vivo, J. Neurooncol., 1, 1, 10.1007/s11060-005-3029-3 · DOI
  32. Pu, 2009, Downregulation of Wnt2 and beta-catenin by siRNA suppresses malignant glioma cell growth, Cancer Gene Ther., 4, 351, 10.1038/cgt.2008.78 · DOI
  33. Sherr, 1996, Cancer cell cycles, Science, 5293, 1672, 10.1126/science.274.5293.1672 · DOI · Paper page
  34. Song, 2009, Galectin-3 mediates nuclear beta-catenin accumulation and Wnt signaling in human colon cancer cells by regulation of glycogen synthase kinase-3beta activity, Cancer Res., 4, 1343, 10.1158/0008-5472.CAN-08-4153 · DOI
  35. Wells, 1999, EGF receptor, Int. J. Biochem. Cell., 6, 637, 10.1016/S1357-2725(99)00015-1 · DOI
  36. Zhang, 2005, The effect of cyclin D expression on cell proliferation in human gliomas, J. Clin. Neurosci., 2, 166, 10.1016/j.jocn.2004.03.036 · DOI
  37. Zhou, 2010, Downregulation of miR-21 inhibits EGFR pathway and suppresses the growth of human glioblastoma cells independent of PTEN status, Lab. Invest., 2, 144, 10.1038/labinvest.2009.126 · DOI

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Metadata

Authors
Han, L., Yang, Y., Yue, X., Huang, K., Liu, X., Pu, P., Jiang, H., Yan, W., Jiang, T., & Kang, C.
Affiliations
  • Tianjin Medical University General Hospital (CN)
  • Second Hospital of Tianjin Medical University (CN)
  • Henry Ford Hospital (US)
  • Capital Medical University (CN)
Corresponding author
  • Jiang, Tao
  • Kang, Chunsheng
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2010-12
Volume
1366
Pages
9-17
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2010.09.097
OpenAlex
W2032563823
Cited by
57
References
1
Citations by year
2026: 3 · 2025: 3 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 4 · 2018: 4 · 2017: 9 · 2016: 2 · 2015: 4 · 2014: 4 · 2013: 6 · 2012: 5
FWCI
2.21
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Key Project of Science and Technology Supporting Programs of China (No. 2007BAI05B08)
  • China National Natural Scientific Fund (30772238, 30772231, 30971136)
  • Program for New Century Excellent Talents in University (NCET-07-0615)
  • Tianjin Science and Technology Committee (09JCZDJC17600)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
Keywords
PI3K/Akt signaling, Wnt/β-catenin signaling, glioblastoma, LY294002, Fra-1, c-Myc, cyclin D1, tumor cell proliferation, tumor invasion, signaling crosstalk, xenograft tumor growth
MeSH terms
Animals, Cell Cycle, Chromones, Disease Models, Animal, Enzyme Inhibitors, Female, Gene Expression Regulation, Glioma, Humans, Mice, Inbred BALB C, Mice, Nude, Morpholines, Serine, Time Factors, Transfection, Signal Transduction, Phosphatidylinositol 3-Kinases, Cell Line, Tumor, Cell Proliferation, Oncogene Protein v-akt, beta Catenin, Mice

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