Molecular cloning and characterization of WNT14B, a novel member of the WNT gene family

Kohno, Hiroyuki; Sekihara, Hisahiko; Katoh, Masaru

doi:10.3892/ijo.19.5.947

Cited by 7 publications

(5 citation statements)

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“…1b): WNT2B [12,13], WNT3 [17,18], WNT3A [18,19], WNT5B [20,21], WNT6 [22], WNT7B [23,24], WNT8A [25,26], WNT8B [26,27], WNT9A (WNT14) [19,28], WNT9B (WNT14B) [28,29] [52], RHOV (ARHV) [53], GIPC2 [54,55], GIPC3 [56], FBXW11 (βTRCP2) [8][9][10]57], SOX17 [58], and TCF7L1 (TCF3) [59]. In 2003, we engaged in dry biology of WNT signaling molecules to identify and characterize PRICKLE1 [60], PRICKLE2 [60], DACT1 (DAPPER1) [61], DACT2 (DAPPER2) [61], DAAM2 [62], and BCL9L [63].…”

Section: Human Wnt-ome Projectmentioning

confidence: 99%

Networking of WNT, FGF, Notch, BMP, and Hedgehog Signaling Pathways during Carcinogenesis

Katoh¹

2007

Stem Cell Rev

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The biological functions of some orthologs within the human genome and model-animal genomes are evolutionarily conserved, but those of others are divergent due to protein evolution and promoter evolution. Because WNT signaling molecules play key roles during embryogenesis, tissue regeneration and carcinogenesis, the author's group has carried out a human WNT-ome project for the comprehensive characterization of human genes encoding WNT signaling molecules. From 1996 to 2002, we cloned and characterized WNT2B/WNT13, WNT3, WNT3A, WNT5B, WNT6, WNT7B, WNT8A, WNT8B, WNT9A/WNT14, WNT9B/WNT14B, WNT10A, WNT10B, WNT11, FZD1, FZD2, FZD3, FZD4, FZD5, FZD6, FZD7, FZD8, FZD10, FRAT1, FRAT2, NKD1, NKD2, VANGL1, RHOU/ARHU, RHOV/ARHV, GIPC2, GIPC3, FBXW11/betaTRCP2, SOX17, TCF7L1/TCF3, and established a cDNA-PCR system for snap-shot and dynamic analyses on the WNT-transcriptome. In 2003, we identified and characterized PRICKLE1, PRICKLE2, DACT1/DAPPER1, DACT2/DAPPER2, DAAM2, and BCL9L. After completion of the human WNT-ome project, we have been working on the stem cell signaling network. WNT signals are transduced to beta-catenin, NLK, NFAT, PKC, JNK and RhoA signaling cascades. FGF20, JAG1 and DKK1 are target genes of the WNT-beta-catenin signaling cascade. Cross-talk of WNT and FGF signaling pathways potentiates beta-catenin and NFAT signaling cascades. BMP signals induce IHH upregulation in co-operation with RUNX. Hedgehog signals induce upregulation of SFRP1, JAG2 and FOXL1, and then FOXL1 induces BMP4 upregulation. The balance between WNT-FGF-Notch and BMP-Hedgehog signaling networks is important for the maintenance of homoestasis among stem and progenitor cells. Disruption of the stem cell signaling network results in pathological conditions, such as congenital diseases and cancer.

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Section: Human Wnt-ome Projectmentioning

confidence: 99%

Networking of WNT, FGF, Notch, BMP, and Hedgehog Signaling Pathways during Carcinogenesis

Katoh¹

2007

Stem Cell Rev

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275

218

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“…WNT3 and WNT9B genes are clustered at human chromosome 17q21.3, while WNT3A and WNT9A genes are clustered at human chromosome 1q42.13. [19][20][21][22] WNT3 and WNT3A as well as WNT9A and WNT9B are paralogs within the human genome. WNT3-WNT9B and WNT3A-WNT9A gene clusters are paralogous regions within the human genome, which are defined as the genomic regions containing thread of paralogs.…”

Section: Genomics On Wnt and Fgf Family Membersmentioning

confidence: 99%

Cross-talk of WNT and FGF signaling pathways at GSK3ß to regulate ß-catenin and SNAIL signaling cascades

Katoh¹,

Katoh²

2006

Cancer Biology & Therapy

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WNT and FGF signaling pathways cross-talk during a variety of cellular processes, such as human colorectal carcinogenesis, mouse mammary tumor virus (MMTV)-induced carcinogenesis, E2A-Pbx-induced leukemogenesis, early embryogenesis, body-axis formation, limb-bud formation, and neurogenesis. Canonical WNT signals are transduced through Frizzled receptor and LRP5/6 coreceptor to downregulate GSK3beta (GSK3B) activity not depending on Ser 9 phosphorylation. FGF signals are transduced through FGF receptor to the FRS2-GRB2-GAB1-PI3K-AKT signaling cascade to downregulate GSK3beta activity depending on Ser 9 phosphorylation. Because GSK3beta-dependent phosphorylation of beta-catenin and SNAIL leads to FBXW1 (betaTRCP)-mediated ubiquitination and degradation, GSK3beta downregulation results in the stabilization and the nuclear accumulation of beta-catenin and SNAIL. Nuclear beta-catenin is complexed with TCF/LEF, Legless (BCL9 or BCL9L) and PYGO (PYGO1 or PYGO2) to activate transcription of CCND1, MYC, FGF18 and FGF20 genes for the cell-fate determination. Nuclear SNAIL represses transcription of CDH1 gene, encoding E-cadherin, to induce the epithelial-mesenchymal transition (EMT). Mammary carcinogenesis in MMTV-Wnt1 transgenic mice is accelerated by MMTV infection due to MMTV integration around Fgf3-Fgf4 or Fgf8 loci, and mammary carcinogenesis in MMTV-Fgf3 transgenic mice due to MMTV integration around Wnt1-Wnt10b locus. Coactivation of WNT and FGF signaling pathways in tumors leads to more malignant phenotypes. Single nucleotide polymorphism (SNP) and copy number polymorphism (CNP) of WNT and FGF signaling molecules could be utilized as screening method of cancer predisposition. cDNA-PCR, microarray or ELISA reflecting aberrant activation of WNT and FGF signaling pathways could be developed as novel cancer-related biomarkers for diagnosis, prognosis, and therapy. Cocktail therapy using WNT and FGF inhibitors, such as small-molecule compounds and human neutralizing antibodies, should be developed to increase the efficacy of chemotherapy through the inhibition of recurrence by destructing cancer stem cells.

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“…Among 19 WNT genes so far identified in human genome, we have previously cloned and characterized WNT2B/WNT13 (1-3), WNT3 (4), WNT3A (5), WNT5B (6), WNT6 (7), WNT7B (8), WNT8A (9), WNT10A (7,10,11), WNT10B (12), WNT11 (13), WNT14 (5,14), and WNT14B (14,15). Proto-oncogene WNT2 is frequently up-regulated in primary gastric cancer and also in primary colorectal cancer (16).…”

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confidence: 99%

WNT2B2 mRNA, Up-Regulated in Primary Gastric Cancer, Is a Positive Regulator of the WNT– β-Catenin–TCF Signaling Pathway

Katoh¹,

Kohno²,

Terasaki

et al. 2001

Biochemical and Biophysical Research Communications

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Molecular cloning and characterization of WNT14B, a novel member of the WNT gene family

Cited by 7 publications

References 0 publications

Networking of WNT, FGF, Notch, BMP, and Hedgehog Signaling Pathways during Carcinogenesis

Networking of WNT, FGF, Notch, BMP, and Hedgehog Signaling Pathways during Carcinogenesis

Cross-talk of WNT and FGF signaling pathways at GSK3ß to regulate ß-catenin and SNAIL signaling cascades

WNT2B2 mRNA, Up-Regulated in Primary Gastric Cancer, Is a Positive Regulator of the WNT– β-Catenin–TCF Signaling Pathway

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