XSIP1, a Xenopus zinc finger/homeodomain encoding gene highly expressed during early neural development

Grunsven, Leo A. van; Papin, Catherine; Avalosse, Bernard; Opdecamp, Karin; Huylebroeck, Danny; Smith, James C.; Bellefroid, Éric

doi:10.1016/s0925-4773(00)00318-x

Cited by 49 publications

(36 citation statements)

References 15 publications

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“…In line with our observations, SIP1 expression has been associated with migratory and invasive mechanisms occurring during embryonic development. Indeed, a high level of SIP1 has been detected during the formation of the neural tube and this has been shown to play a key role in the migration of neural crest cells (Eisaki et al, 2000;van Grunsven et al, 2000;, a system largely described as a physiological archetypal model of EMT (Duband et al, 1995;Tucker, 2004). Also, an increased expression of SIP1 has been described in NMuMG cells which have undergone a TGFβ1-induced EMT characterized by decreased E-cadherin expression and increased N-cadherin expression (Maeda et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

et al. 2006

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The expression of Smad interacting protein-1 (SIP1; ZEB2) and the de novo expression of vimentin are frequently involved in epithelial-to-mesenchynial transitions (EMTs) under both normal and pathological conditions. In the present study, we investigated the potential role of SIP1 in the regulation of vimentin during the EMT associated with breast tumor cell migration and invasion. Examining several breast tumor cell Unes displaying various degrees of invasiveness, we found SIP1 and vimentin expression only in invasive cell Unes. Also, using a model of cell migration with human mammary MCF10A cells, we showed that SIP1 is induced specifically in vimentin-positive migratory cells. Furthermore, transfection of SIP1 cDNA in MCF10A cells increased their vimentin expression both at the mRNA and protein levels and enhanced their migratory abilities in Boyden Chamber assays. Inversely, inhibition of SIP1 expression by RNAi strategies in BT-549 cells and MCF10A cells decreased vimentin expression. We also showed that SIP1 transfection did not activate the TOP-FLASH reporter system, suggesting that the β-catenin/ TCF pathway is not impUcated in the regulation of vimentin by SIP1. Our results therefore impUcate SIP1 in the regulation of vimentin observed in the EMT associated with breast tumor cell migration, a pathway that may contribute to the metastatic progression of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

et al. 2006

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“…The first studies on ZEB2/SIP1 mRNA expression were performed in Xenopus embryos and indicated an important role in early embryogenesis. XSIP1 mRNA is first detected at stage 10.5 (early gastrula) in Xenopus embryos, primarily in dorsal mesoderm and ectoderm [67]. During gastrula and neurula stages, expression persists in neuroectoderm, the neural folds, neural tube, migrating neural crest and lateral plate mesoderm.…”

Section: Key Roles Of Zeb Family Members In Developmentmentioning

confidence: 99%

“…From early tail bud stage on, XdEF1 and XSIP1 are coexpressed in the migratory cranial neural crest, retina and neural tube. In the adult, XSIP1 mRNA is detected in organs derived from ectodermal, mesodermal and endodermal origin, including brain, spinal cord, eye, skin, heart, liver and lung [67]. XSIP1 is known to play an important role in the regulation of Xbra (Xenopus Brachyury), a member of the T-box family of transcription factors and essential in mesoderm formation during early development.…”

Section: Key Roles Of Zeb Family Members In Developmentmentioning

confidence: 99%

The role of the ZEB family of transcription factors in development and disease

Vandewalle

Roy

Berx

2008

Cell. Mol. Life Sci.

431

391

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The ZEB family of zinc finger transcription factors are essential players during normal embryonic development. One characteristic is that they induce epithelial to mesenchymal transition (EMT), a process that reorganizes epithelial cells to become migratory mesenchymal cells. E-cadherin is a major target gene of these transcriptional repressors, and this downregulation is considered a hallmark of EMT. In recent years, the involvement of the ZEB proteins in pathological contexts has been documented as well. Mutations in ZEB encoding genes cause severe syndromic malformations and evidence is mounting that links these factors to malignant tumor progression. In this review, we describe what is currently known on the molecular pathways these transcription factors are implicated in, and we highlight their roles in development and human diseases, with a focus on tumor malignancy.

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“…Smad proteins are signal inducers involved in the TGF-b signaling cascade. XSIP1, the Xenopus homologue of ZFHX1B, is expressed throughout embryogenesis, initially highly expressed in the prospective neuroectoderm and later within the dorsal neural tube and neural crests [van Grunsven et al, 2000]. In early human embryos, ZFHX1B is expressed in neural crest derived cells, including enteric nervous system and the facial neuroectoderm, and the central nervous system, genital tubercle and kidneys [Espinosa-Parrilla et al, 2002].…”

Section: Mutations and Genotype: Phenotype Correlationsmentioning

confidence: 99%

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

Wilson

Mowat

Moal

et al. 2003

American J of Med Genetics Pt A

101

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Mutations or deletions involving ZFHX1B (previously SIP1) have recently been found to cause one form of syndromic Hirschsprung disease (HSCR), associated with microcephaly, mental retardation, and distinctive facial features. Patients with the characteristic facial phenotype and severe mental retardation, but without HSCR, have now also been shown to have mutations in this gene. Mutations of ZFHX1B are frequently associated with other congenital anomalies, including congenital heart disease, hypospadias, renal tract anomalies, and agenesis of the corpus callosum (ACC). We present the clinical data and mutation analysis results from a series of 23 patients with this clinical syndrome, of whom 21 have proven ZFHX1B mutations or deletions (15 previously unpublished). Two patients with the typical features (one with and one without HSCR) did not have detectable abnormalities of ZFHX1B. We emphasize that this syndrome can be recognized by the facial phenotype in the absence of either HSCR or other congenital anomalies, and needs to be considered in the differential diagnosis of dysmorphism with severe mental retardation +/- epilepsy.

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XSIP1, a Xenopus zinc finger/homeodomain encoding gene highly expressed during early neural development

Cited by 49 publications

References 15 publications

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

The role of the ZEB family of transcription factors in development and disease

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

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