Chromosomal localization and cDNA sequence of human BTEB, a GC box binding protein

Ohe, Norihisa; Yamasaki, Yuichi; Sogawa, Kazuhiro; Inazawa, Johji; Ariyama, Takeshi; Oshimura, Mitsuo; Fujii‐Kuriyama, Yoshiaki

doi:10.1007/bf01233255

Cited by 19 publications

(15 citation statements)

References 6 publications

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“…The possible involvement of KLFs in uterine dysfunction as exemplified by endometrial carcinoma initially came from our group’s studies demonstrating cell type-dependent expression of KLF9 (previously designated Basic Transcription Element Binding Protein, BTEB-1; Imataka et al 1992, Ohe et al 1993) in uterine endometrium during pregnancy. We found KLF9 expression predominantly in endometrial stromal cells and to a lesser extent in glandular epithelial cells, with no or undetectable expression in luminal epithelial cells of normal cycling and early pregnant mice (Simmen et al 2004, Velarde et al 2005; Pabona et al 2009).…”

Section: Klfs and Endometrial Carcinomamentioning

confidence: 99%

The emerging role of Krüppel-like factors in endocrine-responsive cancers of female reproductive tissues

Simmen¹,

Pabona²,

Velarde³

et al. 2009

Journal of Endocrinology

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Krüppel-like factors (KLFs), of which there are currently 17 known protein members, belong to the specificity protein (Sp) family of transcription factors and are characterized by the presence of Cys 2 /His 2 zinc finger motifs in their carboxyterminal domains that confer preferential binding to GC/GTrich sequences in gene promoter and enhancer regions. While previously regarded to simply function as silencers of Sp1 transactivity, many KLFs are now shown to be relevant to human cancers by their newly identified abilities to mediate crosstalk with signaling pathways involved in the control of cell proliferation, apoptosis, migration, and differentiation. Several KLFs act as tumor suppressors and/or oncogenes under distinct cellular contexts, underscoring their prognostic potential for cancer survival and outcome. Recent studies suggest that a number of KLFs can influence steroid hormone signaling through transcriptional networks involving steroid hormone receptors and members of the nuclear receptor family of transcription factors. Since inappropriate sensitivity or resistance to steroid hormone actions underlies endocrinerelated malignancies, we consider the intriguing possibility that dysregulation of expression and/or activity of KLF members is linked to the pathogenesis of endometrial and breast cancers. In this review, we focus on recently described mechanisms of actions of several KLFs (KLF4, KLF5, KLF6, and KLF9) in cancers of the mammary gland and uterus. We suggest that understanding the mode of actions of KLFs and their functional networks may lead to the development of novel therapeutics to improve current prospects for cancer prevention and cure.

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Section: Klfs and Endometrial Carcinomamentioning

confidence: 99%

The emerging role of Krüppel-like factors in endocrine-responsive cancers of female reproductive tissues

Simmen¹,

Pabona²,

Velarde³

et al. 2009

Journal of Endocrinology

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“…The full-length human BTEB1 cDNA was isolated by RT-PCR from human endometrial Ishikawa cell RNA using sense (5Ј-ATGTCCGCG-GCCGCCTACAT-3Ј) and antisense (5Ј-TCACAAAGCGTTGGCCA-GCG-3Ј) primer sets corresponding to the reported human BTEB1 cDNA sequence (30), subcloned into the pCRII-TOPO vector (Invitrogen, Carlsbad, CA), and its sequence and orientation confirmed by nucleotide sequence analysis at the Nucleotide Sequencing Facility of the Interdisciplinary Center for Biotechnology Research, University of Florida. The pM and pVP16 chimeric constructs containing the entire coding region of human BTEB1 were generated by releasing the EcoRI insert from the hBTEB1 plasmid DNA and ligating this into the EcoRI site of pM and pVP16 cloning vectors, respectively (CLONTECH Laboratories, Inc., Palo Alto, CA).…”

Section: Plasmids and Expression Constructsmentioning

confidence: 99%

Direct Interaction of the Krüppel-like Family (KLF) Member, BTEB1, and PR Mediates Progesterone-Responsive Gene Expression in Endometrial Epithelial Cells

Zhang

Michel

et al. 2002

Endocrinology

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The present study was undertaken to evaluate the underlying mechanism(s) by which PR and a Krüppel-like family member, basic transcription element binding protein (BTEB1), mediate endometrial epithelial expression of pregnancy-associated genes. Human endometrial carcinoma cell lines (Hec-1-A) expressing high and low levels of BTEB1 were transiently transfected with a human PR isoform (PR-B) expression construct and a luciferase reporter gene driven by the uteroferrin gene promoter that is responsive to both BTEB1 and the PR ligand progesterone. Unliganded PR inhibited luciferase activity in low and high BTEB backgrounds, and this effect was reversed by the synthetic progestin R5020 in both lines. Transactivation by PR of uteroferrin promoter activity (approximately 4-fold) was maximal at lower R5020 concentrations (10 nM) in endometrial cells with higher BTEB1 expression, suggesting that nuclear BTEB1content influenced target gene promoter sensitivity to progesterone. BTEB1 and PR-B were found to physically interact in a progesterone-independent manner, using a coimmunoprecipitation assay that employed antibodies specific to either protein. Moreover, the formation of the BTEB1/PR complex, independent of progesterone, occurred within the context of uterine endometrial proteins and was diminished in late-pregnancy endometrium. Mammalian two-hybrid assays using the entire open reading frame of BTEB1 and/or PR-B fused to either the GAL4 DNA-binding domain or VP16 activation domain and a reporter gene (pG5CAT) under the control of GAL4-binding sites were used to evaluate the formation of functional PR-B/BTEB1 dimer in Cos-1 cells. GAL4/PR-B and VP16/PR-B induced ( approximately 3- to 4-fold) chloramphenicol acetyltransferase (CAT) activity in a progesterone-dependent manner, suggesting PR-dimer formation. By contrast, VP16/PR-B and GAL4/BTEB1 had no effect on basal CAT activity. The combination of VP16- and GAL4-PR-B fusion proteins with the BTEB1 expression construct, pCDNA3-BTEB1 enhanced ligand-bound PR-mediated CAT activity by approximately 3-fold. In transient cotransfection assays using the CAT reporter gene driven by the mouse mammary tumor virus-long terminal repeat promoter, which is responsive to ligand-bound PR but not BTEB1, BTEB1 increased PR-B-mediated CAT activity in a progesterone-dependent manner, consistent with a BTEB1/PR-dimer complex occurring independent of BTEB1 binding to DNA. Unliganded PR-B disrupted the DNA-binding activity of BTEB1 in gel retardation assays, and this effect was enhanced by the presence of PR ligand. Together, these findings support the conclusion that BTEB1 and PR-B are coregulatory proteins that mediate progesterone responsiveness of target genes by direct interactions, leading to the formation of a functional BTEB1/PR-dimer complex.

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“…Kruppel-like factors (KLFs) are the transcription factors that can bind GC-rich sites through three C 2 H 2 -type zinc fingers and regulate diverse biological processes, including development, differentiation, and programmed cell death [8]. KLF9, one of the 17 mammalian KLF family numbers, is also known as basic transcription element-binding protein 1 (BTEB1), which is located at human chromosome 9q13 [8,9]. KLF9 has been shown to control the proliferation of keratinocytes in a daytime-dependent manner [10] and to affect adipocyte differentiation by regulating PPAR g transactivation [11].…”

Section: Introductionmentioning

confidence: 99%

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

Shen

Sun

et al. 2014

Prostate

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Chromosomal localization and cDNA sequence of human BTEB, a GC box binding protein

Cited by 19 publications

References 6 publications

The emerging role of Krüppel-like factors in endocrine-responsive cancers of female reproductive tissues

The emerging role of Krüppel-like factors in endocrine-responsive cancers of female reproductive tissues

Direct Interaction of the Krüppel-like Family (KLF) Member, BTEB1, and PR Mediates Progesterone-Responsive Gene Expression in Endometrial Epithelial Cells

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

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