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WNT Sinyal Yolağı ve Kanser

Yıl 2016, , 27 - 38, 24.06.2016
https://doi.org/10.1501/Ashd_0000000118

Öz

Wnt signaling pathway is critically important in stem cell biology, both in homeostatic maintenance and regeneration of tissues and organs. Aberrant activation of this pathway has been described as a key player in the development of a wide array of tumor types, via affecting the behavior of Cancer Stem Cells (CSCs). CSCs are believed to be responsible for disease relapse, as they possess drug-resistance properties.The development of new therapeutic drugs targeting this pathway topromise new hope to eliminate CSCs and achieve cancer eradication. We review the Wnt signaling pathway, the relationship between this pathway and CSC term and recent therapeutic approaches to target this pathway and their clinical applications

Kaynakça

  • Ahmed, M.A., et al., 2010. CD24 is upregulated in inflammatory bowel disease andstimulates cell motility and colony formation. Inflamm. Bowel. Dis. 16,795–803.
  • Al-Hajj, M., Wicha, M.S., ito-Hernandez, A., Morrison, S.J., Clarke, M.F., 2003.Prospective identification of tumorigenic breast cancer cells. Proc. Natl. Acad.Sci. U. S. A 100, 3983–3988.
  • Baron, J.A., et al., 2003. A randomized trial of aspirin to prevent colorectaladenomas. N. Engl. J. Med. 348, 891–899.
  • Boon, E.M., et al., 2004. Sulindac targets nuclear beta-catenin accumulation andWnt signalling in adenomas of patients with familial adenomatous polyposisand in human colorectal cancer cell lines. Br. J. Cancer 90, 224–229.
  • Bonnet, D., Dick, J.E. 1997. Human acute miyeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 3(7);730-7.
  • Boulais, P.E., Frenette, P.S., 2015. Making sense of hematopoietic stem cell niches.Blood 125, 2621–2629.
  • Bowers, M., et al., 2015. Osteoblast ablation reduces normal long-term hematopoietic stem cell self-renewal but accelerates leukemia development. Blood 125, 2678–2688.
  • Brabletz, T., et al., 2005. Invasion and metastasis in colorectal cancer:epithelial-mesenchymal transition, mesenchymal–epithelial transition, stemcells and beta-catenin. Cells Tissues Organs 179, 56–65.
  • Brudvik, K.W., Paulsen, J.E., Aandahl, E.M., Roald, B., Tasken, K., 2011. Protein kinaseA antagonist inhibits beta-catenin nuclear translocation: c-Myc and COX-2expression and tumor promotion in Apc(Min/+) mice. Mol. Cancer 10, 149.
  • Cadigan, K.M., Liu, Y.I. 2006. Wnt signaling: complexity at the surface. J Cell Sci. 119(Pt 3):395-402.
  • Castellone, M.D., Teramoto, H., Williams, B.O., Druey, K.M., Gutkind, J.S., 2005.Prostaglandin E2 promotes colon cancer cell growth through aGs-axin-beta-catenin signaling axis. Science 310, 1504–1510.
  • Chen X., Yang J., Evans P.M., Liu C. 2008. Wnt signaling: the good and the bad. Acta Biochim Biophys Sin, 40(7); 577-94.
  • Dandekar, S., et al., 2014. Wnt inhibition leads to improved chemosensitivity inpaediatric acute lymphoblastic leukaemia. Br. J. Haematol. 167, 87–99.
  • De, M.C., et al., 2015. Dual cyclooxygenase and carbonic anhydrase inhibition bynonsteroidal anti-inflammatory drugs for the treatment of cancer. Curr. Med.Chem. 22, 2812–2818.
  • DuBois, R.N., Giardiello, F.M., Smalley, W.E., 1996. Nonsteroidal anti-inflammatorydrugs, eicosanoids, and colorectal cancer prevention. Gastroenterol. Clin. NorthAm. 25, 773–791.
  • Duchartrea, Y., KimaY., Kahn M., 2016. The Wnt signaling pathway in cancer. Critical Reviews in Oncology/Hematology 99, 141–149.
  • Espada, J., Moises, B.C., Prado, S.D., Medina, V. 2009. Wnt Signaling and Cancer Stem Cells. Clin Transl Oncol. 11;411-427.
  • Fleming, H.E., et al., 2008. Wnt signaling in the niche enforces hematopoietic stemcell quiescence and is necessary to preserve self-renewal in vivo. Cell Stem Cell2, 274–283.
  • Gang, E.J., et al., 2014. Small-molecule inhibition of CBP/catenin interactionseliminates drug-resistant clones in acute lymphoblastic leukemia. Oncogene33, 2169–2178.
  • Grandy, D., et al., 2009. Discovery and characterization of a small moleculeinhibitor of the PDZ domain of dishevelled. J. Biol. Chem. 284, 16256–16263.
  • Gurney, A., et al., 2012. Wnt pathway inhibition via the targeting of Frizzledreceptors results in decreased growth and tumorigenicity of human tumors.Proc. Natl. Acad. Sci. U. S. A 109, 11717–11722.
  • Han, J., et al., 2012. Small interfering RNA-mediated downregulation ofbeta-catenin inhibits invasion and migration of colon cancer cells in vitro. Med.Sci. Monit. 18, BR273–BR280.
  • Heidel, F.H., et al., 2012. Genetic and pharmacologic inhibition of beta-catenin targets imatinib-resistant leukemia stem cells in CML. Cell Stem Cell 10, 2–424.
  • Huang, S.M., et al., 2009. Tankyrase inhibition stabilizes axin and antagonizes Wntsignalling. Nature 461, 614– 620.Huels, D.J., et al., 2015. E-cadherin can limit the transforming properties ofactivating beta-catenin mutations. EMBO J. 34, 1–2333.
  • Huels, D.J., et al., 2015. E-cadherin can limit the transforming properties ofactivating beta-catenin mutations. EMBO J. 34, 1–2333.
  • Huelsken, J., Beh, Rens, J. 2002. The Wnt signalling pathway. J Cell Sci. 115(21);3977-8.
  • İlyas, M., 2005. Wnt signalling and the mechanistic basis of tumour development. J Pathol. 205(2) ;130–144.
  • Jamieson, C.H., Weissman, I.L., Passegue, E., 2004a. Chronic versus acutemyelogenous leukemia: a question of self-renewal. Cancer Cell 6, 1–533.
  • Jansen, S.R., et al., 2015. Prostaglandin E2 promotes MYCN non-amplifiedneuroblastoma cell survival via beta- catenin stabilization. J. Cell Mol. Med. 19,210–226.
  • Kabiri, Z., et al., 2015. Wnts are dispensable for differentiation and self-renewal ofadult murine hematopoietic stem cells. Blood 126, 1086–1094.
  • Kadowaki, T., Wilder, E., Klingensmith, J., Zachary, K., Perrimon, N., 1996. Thesegment polarity gene porcupine encodes a putative multitransmembraneprotein involved in Wingless processing. Genes Dev. 10, 3116–3128.
  • Kimelman, D., Xu, W., 2006. Beta-catenin destruction complex: insights andquestions from a structural perspective. Oncogene 25, 7482–7491.
  • Kirstetter, P., Anderson, K., Porse, B.T., Jacobsen, S.E., Nerlov, C., 2006. Activation ofthe canonical Wnt pathway leads to loss of hematopoietic stem cellrepopulation and multilineage differentiation block. Nat. Immunol. 7,1048–1056.
  • Klaus, A., Birchmeier, W., 2008. Wnt signalling and its impact on development andcancer. Nat. Rev. Cancer 8, 387–398.Klonisch, T., et al., 2008. Cancer stem cell markers in common cancers— therapeuticimplications. Trends Mol. Med. 14, 450–460.
  • Kode, A., et al., 2015. FoxO1-dependent induction of acute myeloid leukemia by osteoblasts in mice. Leukemia, 161, http://dx.doi.org/10.1038/leu.2015.
  • Kulak, O., et al., 2015. Disruption of Wnt/beta-catenin signaling and telomericshortening are inextricable consequences of tankyrase inhibition in humancells. Mol. Cell Biol. 35, 2425–2435.
  • Lai, S.L., Chien, A.J., Moon, R.T., 2009. Wnt/Fz signaling and the cytoskeleton:potential roles in tumorigenesis. Cell Res. 19, 532–545.Lane, S.W., et al., 2011. Differential niche and Wnt requirements during acutemyeloid leukemia progression. Blood 118, 2849–2856.
  • Lane, S.W., et al., 2011. Differential niche and Wnt requirements during acutemyeloid leukemia progression. Blood 118, 2849–2856.
  • Le, P.N., McDermott, J.D., Jimeno, A., 2015. Targeting the Wnt pathway in humancancers: therapeutic targeting with a focus on OMP-54F28. Pharmacol. Ther.146, 1–11.
  • Luis, T.C., Ichii, M., Brugman, M.H., Kincade, P., Staal, F.J., 2012. Wnt signalingstrength regulates normal hematopoiesis and its deregulation is involved inleukemia development. Leukemia 26, 414–421.
  • Madan, B., et al., 2015. Wnt addiction of genetically defined cancers reversed byPORCN inhibition. Oncogene.
  • Manabe, A., Coustan-Smith, E., Behm, F.G., Raimondi, S.C., Campana, D., 1992. Bonemarrow-derived stromal cells prevent apoptotic cell death in B-lineage acutelymphoblastic leukemia. Blood 79, 2370–2377.
  • Meads, M.B., Gatenby, R.A., Dalton, W.S., 2009. Environment-mediated drugresistance: a major contributor to minimal residual disease. Nat. Rev. Cancer 9,665–674.
  • Mikels, A.J, Nusse, R. 2006. Wnts as ligands: processing, secretion and reception. Oncogene 25(57):7461-8.
  • Moon, R.T., 2005. Wnt/beta-catenin pathway. Sci. STKE, cm1.
  • Nusse, R. 2005. Wnt signaling in disease and in development. Cell Res 15(1) ;28-32.
  • Nusse, R., Varmus, H.E. 1992. Wnt genes. Cell. 69(7) ;1073-87.
  • Palmer, H.G., et al., 2001. Vitamin D(3) promotes the differentiation of coloncarcinoma cells by the induction of E-cadherin and the inhibition ofbeta-catenin signaling. J. Cell Biol. 154, 369–387.
  • Phillips, R.K., et al., 2002. A randomised, double blind, placebo controlled study ofcelecoxib, a selective cyclooxygenase 2 inhibitor, on duodenal polyposis infamilial adenomatous polyposis. Gut 50, 857–860.
  • Reya, T., Morrison, S.J., Clarke, M.F., Weissman, I.L., 2001. Stem cells, cancer, andcancer stem cells. Nature 414, 105–111.
  • Rios-Esteves, J., Resh, M.D., 2013. Stearoyl CoA desaturase is required to produceactive, lipid-modified Wnt proteins. Cell Rep. 4, 1072–1081.
  • Sandler, R.S., et al., 2003. A randomized trial of aspirin to prevent colorectaladenomas in patients with previous colorectal cancer. N. Engl. J. Med. 348,883–890.
  • Schambony, A., Wedlich, D., 2007. Wnt-5A/Ror2 regulate expression of XPAPCthrough an alternative noncanonical signaling pathway. Dev. Cell 12, 779–792.
  • Schmitt, M., Metzger, M., Gradl, D., Davidson, G., Orian-Rousseau, V., 2015. CD44functions in Wnt signaling by regulating LRP6 localization and activation. CellDeath. Differ. 22, 677–689.
  • Schurch, C., Riether, C., Matter, M.S., Tzankov, A., Ochsenbein, A.F., 2012. CD27signaling on chronic myelogenous leukemia stem cells activates Wnt targetgenes and promotes disease progression. J. Clin. Invest. 122, 624–638.
  • Shulewitz, M., et al., 2006. Repressor roles for TCF-4 and Sfrp1 in Wnt signaling inbreast cancer. Oncogene 25, 4361–4369.
  • Smith, et al., 2013. J. Clin. Oncol. 31 (suppl; abstr 2540).Steinbach, G., et al., 2000. The effect of celecoxib, a cyclooxygenase-2 inhibitor, infamilial adenomatous polyposis. N. Engl. J. Med. 342, 1946–1952.
  • Steinbach, G., et al., 2000. The effect of celecoxib, a cyclooxygenase-2 inhibitor, infamilial adenomatous polyposis. N. Engl. J. Med. 342, 1946–1952.
  • Teo, J.L., Kahn, M., 2010. The Wnt signaling pathway in cellular proliferation anddifferentiation: a tale of two coactivators. Adv. Drug Deliv. Rev. 62, 1149–1155.
  • Thun, M.J., Henley, S.J., Patrono, C., 2002. Nonsteroidal anti-inflammatory drugs asanticancer agents: mechanistic, pharmacologic, and clinical issues. J. Natl.Cancer Inst. 94, 252–266.
  • Valencia, A., et al., 2009. Wnt signaling pathway is epigenetically regulated bymethylation of Wnt antagonists in acute myeloid leukemia. Leukemia 23,1658–1666.
  • Van, A.R., Nusse, R., 2009. Towards an integrated view of Wnt signaling indevelopment. Development 136, 3205–3214.
  • Veeman, M.T., Axelrod, J.D., Moon, R.T., 2003. A second canon. Functions andmechanisms of beta-catenin- independent Wnt signaling. Dev. Cell 5, 367–377.
  • Wang, Y., et al., 2010. The Wnt/beta-catenin pathway is required for thedevelopment of leukemia stem cells in AML. Science 327, 1650–1653.
  • Willert, K., Jones, K.A., 2006. Wnt signaling: is the party in the nucleus? Genes Dev.20, 1394–1404.
  • Williams, J.L., et al., 2001. Nitric oxide-releasing nonsteroidal anti-inflammatorydrugs (NSAIDs) alter the kinetics of human colon cancer cell lines moreeffectively than traditional NSAIDs: implications for colon cancerchemoprevention. Cancer Res. 61, 3285–3289.
  • Williams, J.L., et al., 2004. NO-donating aspirin inhibits intestinal carcinogenesis inMin (APC(Min/+)) mice. Biochem. Biophys. Res. Commun. 313, 784–788.
  • Xiao, J.H., et al., 2003. Adenomatous polyposis coli (APC)-independent regulationof beta-catenin degradation via a retinoid X receptor-mediated pathway. J.Biol. Chem. 278, 29954–29962.
  • Yamada, T., et al., 2000. Transactivation of the multidrug resistance 1 gene byT-cell factor 4/beta-catenin complex in early colorectal carcinogenesis. CancerRes. 60, 4761–4766.
  • Yamamoto, S., et al., 2008. Cthrc1 selectively activates the planar cell polaritypathway of Wnt signaling by stabilizing the Wnt-receptor complex. Dev. Cell15, 23–36.
  • Yang, K., et al., 2003. Regional response leading to tumorigenesis after sulindac insmall and large intestine of mice with Apc mutations. Carcinogenesis 24,605–611.
  • Zhang, B., et al., 2013. Microenvironmental protection of CML stem and progenitorcells from tyrosine kinase
  • inhibitors through N-cadherin andWnt-beta-catenin signaling. Blood 121, 1824–1838.

Wnt sinyal yolağı ve kanser

Yıl 2016, , 27 - 38, 24.06.2016
https://doi.org/10.1501/Ashd_0000000118

Öz

Wnt sinyal yolağı kök hücre biyolojisinde, doku ve organ rejenerasyonunda ve homeostatik devamlılığın sağlanmasında kritik bir öneme sahiptir. Bu yolağın anormal aktivasyonunun pek çok tümör tipinin gelişiminde anahtar bir rol oynadığı ve bu durumun kanser kök hücrelerin (KKH, cancer stem cell=CSC) davranışını etkilediği bilinmektedir. KKH’ler ilaca direnç gösterebilme özelliğinden dolayı hastalıkların nüks etmesinin temel nedeni olduğu düşünülmektedir. Wnt sinyal yolağını hedef alan yeni terapötik ilaçların keşfedilmesi, KKH’lerin elimine edilmesine ve kanserin yok edilmesine yönelik yeni umutlar vaat etmektedir. Bu derleme de Wnt sinyal yolağı, bu yolağın kanser kök hücre kavramı ile ilişkisi ve klinik uygulamalarını hedef alan yakın zamandaki terapötik yaklaşımlar tartışılmıştır

Kaynakça

  • Ahmed, M.A., et al., 2010. CD24 is upregulated in inflammatory bowel disease andstimulates cell motility and colony formation. Inflamm. Bowel. Dis. 16,795–803.
  • Al-Hajj, M., Wicha, M.S., ito-Hernandez, A., Morrison, S.J., Clarke, M.F., 2003.Prospective identification of tumorigenic breast cancer cells. Proc. Natl. Acad.Sci. U. S. A 100, 3983–3988.
  • Baron, J.A., et al., 2003. A randomized trial of aspirin to prevent colorectaladenomas. N. Engl. J. Med. 348, 891–899.
  • Boon, E.M., et al., 2004. Sulindac targets nuclear beta-catenin accumulation andWnt signalling in adenomas of patients with familial adenomatous polyposisand in human colorectal cancer cell lines. Br. J. Cancer 90, 224–229.
  • Bonnet, D., Dick, J.E. 1997. Human acute miyeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 3(7);730-7.
  • Boulais, P.E., Frenette, P.S., 2015. Making sense of hematopoietic stem cell niches.Blood 125, 2621–2629.
  • Bowers, M., et al., 2015. Osteoblast ablation reduces normal long-term hematopoietic stem cell self-renewal but accelerates leukemia development. Blood 125, 2678–2688.
  • Brabletz, T., et al., 2005. Invasion and metastasis in colorectal cancer:epithelial-mesenchymal transition, mesenchymal–epithelial transition, stemcells and beta-catenin. Cells Tissues Organs 179, 56–65.
  • Brudvik, K.W., Paulsen, J.E., Aandahl, E.M., Roald, B., Tasken, K., 2011. Protein kinaseA antagonist inhibits beta-catenin nuclear translocation: c-Myc and COX-2expression and tumor promotion in Apc(Min/+) mice. Mol. Cancer 10, 149.
  • Cadigan, K.M., Liu, Y.I. 2006. Wnt signaling: complexity at the surface. J Cell Sci. 119(Pt 3):395-402.
  • Castellone, M.D., Teramoto, H., Williams, B.O., Druey, K.M., Gutkind, J.S., 2005.Prostaglandin E2 promotes colon cancer cell growth through aGs-axin-beta-catenin signaling axis. Science 310, 1504–1510.
  • Chen X., Yang J., Evans P.M., Liu C. 2008. Wnt signaling: the good and the bad. Acta Biochim Biophys Sin, 40(7); 577-94.
  • Dandekar, S., et al., 2014. Wnt inhibition leads to improved chemosensitivity inpaediatric acute lymphoblastic leukaemia. Br. J. Haematol. 167, 87–99.
  • De, M.C., et al., 2015. Dual cyclooxygenase and carbonic anhydrase inhibition bynonsteroidal anti-inflammatory drugs for the treatment of cancer. Curr. Med.Chem. 22, 2812–2818.
  • DuBois, R.N., Giardiello, F.M., Smalley, W.E., 1996. Nonsteroidal anti-inflammatorydrugs, eicosanoids, and colorectal cancer prevention. Gastroenterol. Clin. NorthAm. 25, 773–791.
  • Duchartrea, Y., KimaY., Kahn M., 2016. The Wnt signaling pathway in cancer. Critical Reviews in Oncology/Hematology 99, 141–149.
  • Espada, J., Moises, B.C., Prado, S.D., Medina, V. 2009. Wnt Signaling and Cancer Stem Cells. Clin Transl Oncol. 11;411-427.
  • Fleming, H.E., et al., 2008. Wnt signaling in the niche enforces hematopoietic stemcell quiescence and is necessary to preserve self-renewal in vivo. Cell Stem Cell2, 274–283.
  • Gang, E.J., et al., 2014. Small-molecule inhibition of CBP/catenin interactionseliminates drug-resistant clones in acute lymphoblastic leukemia. Oncogene33, 2169–2178.
  • Grandy, D., et al., 2009. Discovery and characterization of a small moleculeinhibitor of the PDZ domain of dishevelled. J. Biol. Chem. 284, 16256–16263.
  • Gurney, A., et al., 2012. Wnt pathway inhibition via the targeting of Frizzledreceptors results in decreased growth and tumorigenicity of human tumors.Proc. Natl. Acad. Sci. U. S. A 109, 11717–11722.
  • Han, J., et al., 2012. Small interfering RNA-mediated downregulation ofbeta-catenin inhibits invasion and migration of colon cancer cells in vitro. Med.Sci. Monit. 18, BR273–BR280.
  • Heidel, F.H., et al., 2012. Genetic and pharmacologic inhibition of beta-catenin targets imatinib-resistant leukemia stem cells in CML. Cell Stem Cell 10, 2–424.
  • Huang, S.M., et al., 2009. Tankyrase inhibition stabilizes axin and antagonizes Wntsignalling. Nature 461, 614– 620.Huels, D.J., et al., 2015. E-cadherin can limit the transforming properties ofactivating beta-catenin mutations. EMBO J. 34, 1–2333.
  • Huels, D.J., et al., 2015. E-cadherin can limit the transforming properties ofactivating beta-catenin mutations. EMBO J. 34, 1–2333.
  • Huelsken, J., Beh, Rens, J. 2002. The Wnt signalling pathway. J Cell Sci. 115(21);3977-8.
  • İlyas, M., 2005. Wnt signalling and the mechanistic basis of tumour development. J Pathol. 205(2) ;130–144.
  • Jamieson, C.H., Weissman, I.L., Passegue, E., 2004a. Chronic versus acutemyelogenous leukemia: a question of self-renewal. Cancer Cell 6, 1–533.
  • Jansen, S.R., et al., 2015. Prostaglandin E2 promotes MYCN non-amplifiedneuroblastoma cell survival via beta- catenin stabilization. J. Cell Mol. Med. 19,210–226.
  • Kabiri, Z., et al., 2015. Wnts are dispensable for differentiation and self-renewal ofadult murine hematopoietic stem cells. Blood 126, 1086–1094.
  • Kadowaki, T., Wilder, E., Klingensmith, J., Zachary, K., Perrimon, N., 1996. Thesegment polarity gene porcupine encodes a putative multitransmembraneprotein involved in Wingless processing. Genes Dev. 10, 3116–3128.
  • Kimelman, D., Xu, W., 2006. Beta-catenin destruction complex: insights andquestions from a structural perspective. Oncogene 25, 7482–7491.
  • Kirstetter, P., Anderson, K., Porse, B.T., Jacobsen, S.E., Nerlov, C., 2006. Activation ofthe canonical Wnt pathway leads to loss of hematopoietic stem cellrepopulation and multilineage differentiation block. Nat. Immunol. 7,1048–1056.
  • Klaus, A., Birchmeier, W., 2008. Wnt signalling and its impact on development andcancer. Nat. Rev. Cancer 8, 387–398.Klonisch, T., et al., 2008. Cancer stem cell markers in common cancers— therapeuticimplications. Trends Mol. Med. 14, 450–460.
  • Kode, A., et al., 2015. FoxO1-dependent induction of acute myeloid leukemia by osteoblasts in mice. Leukemia, 161, http://dx.doi.org/10.1038/leu.2015.
  • Kulak, O., et al., 2015. Disruption of Wnt/beta-catenin signaling and telomericshortening are inextricable consequences of tankyrase inhibition in humancells. Mol. Cell Biol. 35, 2425–2435.
  • Lai, S.L., Chien, A.J., Moon, R.T., 2009. Wnt/Fz signaling and the cytoskeleton:potential roles in tumorigenesis. Cell Res. 19, 532–545.Lane, S.W., et al., 2011. Differential niche and Wnt requirements during acutemyeloid leukemia progression. Blood 118, 2849–2856.
  • Lane, S.W., et al., 2011. Differential niche and Wnt requirements during acutemyeloid leukemia progression. Blood 118, 2849–2856.
  • Le, P.N., McDermott, J.D., Jimeno, A., 2015. Targeting the Wnt pathway in humancancers: therapeutic targeting with a focus on OMP-54F28. Pharmacol. Ther.146, 1–11.
  • Luis, T.C., Ichii, M., Brugman, M.H., Kincade, P., Staal, F.J., 2012. Wnt signalingstrength regulates normal hematopoiesis and its deregulation is involved inleukemia development. Leukemia 26, 414–421.
  • Madan, B., et al., 2015. Wnt addiction of genetically defined cancers reversed byPORCN inhibition. Oncogene.
  • Manabe, A., Coustan-Smith, E., Behm, F.G., Raimondi, S.C., Campana, D., 1992. Bonemarrow-derived stromal cells prevent apoptotic cell death in B-lineage acutelymphoblastic leukemia. Blood 79, 2370–2377.
  • Meads, M.B., Gatenby, R.A., Dalton, W.S., 2009. Environment-mediated drugresistance: a major contributor to minimal residual disease. Nat. Rev. Cancer 9,665–674.
  • Mikels, A.J, Nusse, R. 2006. Wnts as ligands: processing, secretion and reception. Oncogene 25(57):7461-8.
  • Moon, R.T., 2005. Wnt/beta-catenin pathway. Sci. STKE, cm1.
  • Nusse, R. 2005. Wnt signaling in disease and in development. Cell Res 15(1) ;28-32.
  • Nusse, R., Varmus, H.E. 1992. Wnt genes. Cell. 69(7) ;1073-87.
  • Palmer, H.G., et al., 2001. Vitamin D(3) promotes the differentiation of coloncarcinoma cells by the induction of E-cadherin and the inhibition ofbeta-catenin signaling. J. Cell Biol. 154, 369–387.
  • Phillips, R.K., et al., 2002. A randomised, double blind, placebo controlled study ofcelecoxib, a selective cyclooxygenase 2 inhibitor, on duodenal polyposis infamilial adenomatous polyposis. Gut 50, 857–860.
  • Reya, T., Morrison, S.J., Clarke, M.F., Weissman, I.L., 2001. Stem cells, cancer, andcancer stem cells. Nature 414, 105–111.
  • Rios-Esteves, J., Resh, M.D., 2013. Stearoyl CoA desaturase is required to produceactive, lipid-modified Wnt proteins. Cell Rep. 4, 1072–1081.
  • Sandler, R.S., et al., 2003. A randomized trial of aspirin to prevent colorectaladenomas in patients with previous colorectal cancer. N. Engl. J. Med. 348,883–890.
  • Schambony, A., Wedlich, D., 2007. Wnt-5A/Ror2 regulate expression of XPAPCthrough an alternative noncanonical signaling pathway. Dev. Cell 12, 779–792.
  • Schmitt, M., Metzger, M., Gradl, D., Davidson, G., Orian-Rousseau, V., 2015. CD44functions in Wnt signaling by regulating LRP6 localization and activation. CellDeath. Differ. 22, 677–689.
  • Schurch, C., Riether, C., Matter, M.S., Tzankov, A., Ochsenbein, A.F., 2012. CD27signaling on chronic myelogenous leukemia stem cells activates Wnt targetgenes and promotes disease progression. J. Clin. Invest. 122, 624–638.
  • Shulewitz, M., et al., 2006. Repressor roles for TCF-4 and Sfrp1 in Wnt signaling inbreast cancer. Oncogene 25, 4361–4369.
  • Smith, et al., 2013. J. Clin. Oncol. 31 (suppl; abstr 2540).Steinbach, G., et al., 2000. The effect of celecoxib, a cyclooxygenase-2 inhibitor, infamilial adenomatous polyposis. N. Engl. J. Med. 342, 1946–1952.
  • Steinbach, G., et al., 2000. The effect of celecoxib, a cyclooxygenase-2 inhibitor, infamilial adenomatous polyposis. N. Engl. J. Med. 342, 1946–1952.
  • Teo, J.L., Kahn, M., 2010. The Wnt signaling pathway in cellular proliferation anddifferentiation: a tale of two coactivators. Adv. Drug Deliv. Rev. 62, 1149–1155.
  • Thun, M.J., Henley, S.J., Patrono, C., 2002. Nonsteroidal anti-inflammatory drugs asanticancer agents: mechanistic, pharmacologic, and clinical issues. J. Natl.Cancer Inst. 94, 252–266.
  • Valencia, A., et al., 2009. Wnt signaling pathway is epigenetically regulated bymethylation of Wnt antagonists in acute myeloid leukemia. Leukemia 23,1658–1666.
  • Van, A.R., Nusse, R., 2009. Towards an integrated view of Wnt signaling indevelopment. Development 136, 3205–3214.
  • Veeman, M.T., Axelrod, J.D., Moon, R.T., 2003. A second canon. Functions andmechanisms of beta-catenin- independent Wnt signaling. Dev. Cell 5, 367–377.
  • Wang, Y., et al., 2010. The Wnt/beta-catenin pathway is required for thedevelopment of leukemia stem cells in AML. Science 327, 1650–1653.
  • Willert, K., Jones, K.A., 2006. Wnt signaling: is the party in the nucleus? Genes Dev.20, 1394–1404.
  • Williams, J.L., et al., 2001. Nitric oxide-releasing nonsteroidal anti-inflammatorydrugs (NSAIDs) alter the kinetics of human colon cancer cell lines moreeffectively than traditional NSAIDs: implications for colon cancerchemoprevention. Cancer Res. 61, 3285–3289.
  • Williams, J.L., et al., 2004. NO-donating aspirin inhibits intestinal carcinogenesis inMin (APC(Min/+)) mice. Biochem. Biophys. Res. Commun. 313, 784–788.
  • Xiao, J.H., et al., 2003. Adenomatous polyposis coli (APC)-independent regulationof beta-catenin degradation via a retinoid X receptor-mediated pathway. J.Biol. Chem. 278, 29954–29962.
  • Yamada, T., et al., 2000. Transactivation of the multidrug resistance 1 gene byT-cell factor 4/beta-catenin complex in early colorectal carcinogenesis. CancerRes. 60, 4761–4766.
  • Yamamoto, S., et al., 2008. Cthrc1 selectively activates the planar cell polaritypathway of Wnt signaling by stabilizing the Wnt-receptor complex. Dev. Cell15, 23–36.
  • Yang, K., et al., 2003. Regional response leading to tumorigenesis after sulindac insmall and large intestine of mice with Apc mutations. Carcinogenesis 24,605–611.
  • Zhang, B., et al., 2013. Microenvironmental protection of CML stem and progenitorcells from tyrosine kinase
  • inhibitors through N-cadherin andWnt-beta-catenin signaling. Blood 121, 1824–1838.
Toplam 73 adet kaynakça vardır.

Ayrıntılar

Diğer ID JA88AF89TZ
Bölüm Araştırma Makalesi
Yazarlar

Buket Altınok Bu kişi benim

Asuman Sunguroğlu Bu kişi benim

Yayımlanma Tarihi 24 Haziran 2016
Gönderilme Tarihi 1 Ekim 2016
Yayımlandığı Sayı Yıl 2016

Kaynak Göster

APA Altınok, B., & Sunguroğlu, A. (2016). Wnt sinyal yolağı ve kanser. Ankara Sağlık Hizmetleri Dergisi, 15(2), 27-38. https://doi.org/10.1501/Ashd_0000000118
AMA Altınok B, Sunguroğlu A. Wnt sinyal yolağı ve kanser. ASHD. Haziran 2016;15(2):27-38. doi:10.1501/Ashd_0000000118
Chicago Altınok, Buket, ve Asuman Sunguroğlu. “Wnt Sinyal yolağı Ve Kanser”. Ankara Sağlık Hizmetleri Dergisi 15, sy. 2 (Haziran 2016): 27-38. https://doi.org/10.1501/Ashd_0000000118.
EndNote Altınok B, Sunguroğlu A (01 Haziran 2016) Wnt sinyal yolağı ve kanser. Ankara Sağlık Hizmetleri Dergisi 15 2 27–38.
IEEE B. Altınok ve A. Sunguroğlu, “Wnt sinyal yolağı ve kanser”, ASHD, c. 15, sy. 2, ss. 27–38, 2016, doi: 10.1501/Ashd_0000000118.
ISNAD Altınok, Buket - Sunguroğlu, Asuman. “Wnt Sinyal yolağı Ve Kanser”. Ankara Sağlık Hizmetleri Dergisi 15/2 (Haziran 2016), 27-38. https://doi.org/10.1501/Ashd_0000000118.
JAMA Altınok B, Sunguroğlu A. Wnt sinyal yolağı ve kanser. ASHD. 2016;15:27–38.
MLA Altınok, Buket ve Asuman Sunguroğlu. “Wnt Sinyal yolağı Ve Kanser”. Ankara Sağlık Hizmetleri Dergisi, c. 15, sy. 2, 2016, ss. 27-38, doi:10.1501/Ashd_0000000118.
Vancouver Altınok B, Sunguroğlu A. Wnt sinyal yolağı ve kanser. ASHD. 2016;15(2):27-38.