Differential expression of canonical and non-canonical Wnt ligands in ameloblastoma

Siar, C.H. and Nagatsuka, H. and Han, P.P. and Buery, R.R. and Tsujigiwa, H. and Nakano, K. and Ng, K.H. and Kawakami, T. (2012) Differential expression of canonical and non-canonical Wnt ligands in ameloblastoma. Journal of Oral Pathology & Medicine, 41 (4). pp. 332-339. ISSN 0904-2512


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BACKGROUND: Canonical and non-canonical Wnt signaling pathways modulate diverse cellular processes during embryogenesis and post-natally. Their deregulations have been implicated in cancer development and progression. Wnt signaling is essential for odontogenesis. The ameloblastoma is an odontogenic epithelial neoplasm of enamel organ origin. Altered expressions of Wnts-1, -2, -5a, and -10a are detected in this tumor. The activity of other Wnt members remains unclarified. MATERIALS AND METHODS: Canonical (Wnts-1, -2, -3, -8a, -8b, -10a, and -10b), non-canonical (Wnts-4, -5a, -5b, -6, 7a, -7b, and -11), and indeterminate groups (Wnts-2b and -9b) were examined immunohistochemically in 72 cases of ameloblastoma (19 unicystic UA, 35 solid/multicystic SMA, eight desmoplastic DA, and 10 recurrent RA). RESULTS: Canonical Wnt proteins (except Wnt-10b) were heterogeneously expressed in ameloblastoma. Their distribution patterns were distinctive with some overlap. Protein localization was mainly membranous and/or cytoplasmic. Overexpression of Wnt-1 in most subsets (UA = 19/19; SMA = 35/35; DA = 5/8; RA = 7/10) (P < 0.05), Wnt-3 in granular cell variant (n = 3/ 3), and Wnt-8b in DA (n = 8/ 8) was key observations. Wnts-8a and -10a demonstrated enhanced expression in tumoral buddings and acanthomatous areas. Noncanonical and indeterminate Wnts were absent except for limited Wnt-7b immunoreactivity in UA (n = 1/ 19) and SMA (n = 1/ 35). Stromal components expressed variable Wnt positivity. CONCLUSION: Differential expression of Wnt ligands in different ameloblastoma subtypes suggests that the canonical and non-canonical Wnt pathways are selectively activated or repressed depending on the tumor cell differentiation status. Canonical Wnt pathway is most likely the main transduction pathway while Wnt-1 might be the key signaling molecule involved in ameloblastoma tumorigenesis. J Oral Pathol Med (2012) 41: 332-339

Item Type: Article
Additional Information: ISI Document Delivery No.: 910OZ Times Cited: 0 Cited Reference Count: 44 Cited References: Barbolina MV, 2011, BIOCHEM J, V437, P1, DOI 10.1042/BJ20110112 Bohring A, 2009, AM J HUM GENET, V85, P97, DOI 10.1016/j.ajhg.2009.06.001 Bui T. D., 1998, British Journal of Cancer, V77, P319, DOI 10.1038/bjc.1998.49 Camilli TC, 2010, BIOCHEM PHARMACOL, V80, P702, DOI 10.1016/j.bcp.2010.03.002 Chen X, 2008, ACTA BIOCH BIOPH SIN, V40, P577, DOI 10.1111/j.1745-7270.2008.00440.x Cheng XX, 2005, CANCER LETT, V223, P339, DOI 10.1016/j.canlet.2004.11.013 Chuah KS, 2009, J HARD TISSUE BIOL, V18, P63 DeVilliers P, 2011, J DENT RES, V90, P463, DOI 10.1177/0022034510391791 Gardner DG, 2005, WHO CLASSIFICATION T, P296 Hakim SG, 2011, CLIN ORAL INVEST, V15, P321, DOI 10.1007/s00784-010-0388-8 He B, 2004, NEOPLASIA, V6, P7 HINCK L, 1994, J CELL BIOL, V124, P729, DOI 10.1083/jcb.124.5.729 Hirohashi S, 2003, CANCER SCI, V94, P575, DOI 10.1111/j.1349-7006.2003.tb01485.x Khor TO, 2006, INT J COLORECTAL DIS, V21, P291, DOI 10.1007/s00384-005-0002-8 Kim SA, 2007, ORAL SURG ORAL MED O, V103, P97, DOI 10.1016/j.tripleo.2005.10.037 Kumamoto H, 2001, J ORAL PATHOL MED, V30, P309, DOI 10.1034/j.1600-0714.2001.300509.x Kumamoto H, 2005, J ORAL PATHOL MED, V34, P401, DOI 10.1111/j.1600-0714.2005.00328.x Leocata P, 2007, J ORAL PATHOL MED, V36, P394, DOI 10.1111/j.1600-0714.2007.00537.x Liu F, 2010, J DENT RES, V89, P318, DOI 10.1177/0022034510363373 Luo HY, 2006, INT J ORAL MAX SURG, V35, P750, DOI 10.1016/j.ijom.2006.03.012 Lv J, 2010, GENET TEST MOL BIOMA, V14, P363, DOI 10.1089/gtmb.2009.0173 Miletich I, 2003, HUM MOL GENET, V12, pR69, DOI 10.1093/hmg/ddg085 NG KH, 1990, ORAL SURG ORAL MED O, V70, P210, DOI 10.1016/0030-4220(90)90121-8 NG KH, 1993, BRIT J ORAL MAX SURG, V31, P299, DOI 10.1016/0266-4356(93)90064-4 PAPKOFF J, 1990, MOL CELL BIOL, V10, P2723 Pereira KMA, 2010, ORAL SURG ORAL MED O, V109, P425, DOI 10.1016/j.tripleo.2009.10.032 Ridgway LD, 2011, EXP THER MED, V2, P229, DOI 10.3892/etm.2010.189 Sandra F, 2001, HISTOPATHOLOGY, V39, P93, DOI 10.1046/j.1365-2559.2001.01138.x Sarkar L, 1999, MECH DEVELOP, V85, P197, DOI 10.1016/S0925-4773(99)00095-7 Sathi Gul San Ara, 2007, J Oral Pathol Med, V36, P609 Sekine S, 2003, AM J PATHOL, V163, P1707, DOI 10.1016/S0002-9440(10)63528-6 SIAR CH, 1993, BRIT J ORAL MAX SURG, V31, P183, DOI 10.1016/0266-4356(93)90122-D Siar CH, 2010, J ORAL PATHOL MED, V39, P552, DOI 10.1111/j.1600-0714.2009.00871.x Siriwardena BSMS, 2009, ORAL ONCOL, V45, P103, DOI 10.1016/j.oraloncology.2008.03.008 Sukarawan W, 2010, AM J PATHOL, V176, P461, DOI 10.2353/ajpath.2010.090478 Tanahashi J, 2008, J ORAL PATHOL MED, V37, P565, DOI 10.1111/j.1600-0714.2008.00645.x Tanaka A, 2007, J ORAL PATHOL MED, V34, P400 Thesleff I, 1997, MECH DEVELOP, V67, P111, DOI 10.1016/S0925-4773(97)00115-9 Tsujigiwa H, 2005, ORAL ONCOL, V41, P843, DOI 10.1016/j.oraloncology.2005.04.005 Xiao J, 2007, J HARD TISSUE BIOL, V16, P79, DOI 10.2485/jhtb.16.79 Yamashiro T, 2007, DIFFERENTIATION, V75, P452, DOI 10.1111/j.1432-0436.2006.00150.x You L, 2004, ONCOGENE, V23, P6170, DOI 10.1038/sj.onc.1207844 Yuzugullu H, 2009, MOL CANCER, V8, DOI 10.1186/1476-4598-8-90 Zhang WM, 2005, ONCOL REP, V13, P1095 Siar, Chong Huat Nagatsuka, Hitoshi Han, Phuu Pwint Buery, Rosario Rivera Tsujigiwa, Hidetsugu Nakano, Keisuke Ng, Kok Han Kawakami, Toshiyuki University of MalayaRG083/09HTM; Japan Society for the Promotion of Science20592349 This study is jointly funded by the University of Malaya Research Grant RG083/09HTM and Grant-in-Aid for Scientific Research (C) (20592349) from the Japan Society for the Promotion of Science. We are grateful to Mrs. Khoo Guat Sim, Mrs. Rusnani Kamal, Mrs. Siti Nurull Huda Ariffin, Mrs. Hasilah Mokhtar, and Mr. Richee Rudeen Yasib for their technical support. Wiley-blackwell Malden
Uncontrolled Keywords: Ameloblastoma canonical immunohistochemistry non-canonical Wnt adenomatous polyposis-coli squamous-cell carcinoma beta-catenin expression wingless-type protein-1 dental development cancer-cells tumor gene morphogenesis apoptosis
Subjects: R Medicine > RK Dentistry
Divisions: Faculty of Dentistry > Dept of Oral Pathology & Oral Medicine & Periodontology
Depositing User: Ms Nursyafiqah Abd Malek
Date Deposited: 10 Jan 2013 00:23
Last Modified: 10 Jan 2013 00:23
URI: http://eprints.um.edu.my/id/eprint/4329

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