SATB Homeobox Proteins Regulate Trophoblast Stem Cell Renewal and Differentiation

Asanoma, Kazuo; Kubota, Kaiyu; Chakraborty, Damayanti; Renaud, Stephen J.; Wake, Norio; Fukushima, Kotaro; Soares, Michael J.; Rumi, M.A. Karim

doi:10.1074/jbc.m111.287128

Cited by 50 publications

(73 citation statements)

References 69 publications

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“…For example, the chromatin organizers SATB homeobox 1 (SATB1) and SATB2 have been shown to be essential for maintaining a stem-cell identity within rat TSCs (Asanoma, et al 2012). Mechanistic analyses showed that loss of SATB proteins in TSCs resulted in reduced expression of Eomes and loss of TSC self-renewal.…”

Section: Chromatin Remodeling Factors and Trophoblast Developmentmentioning

confidence: 99%

Transcriptional regulators of the trophoblast lineage in mammals with hemochorial placentation

Knott¹,

Paul²

2014

Reproduction

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Mammalian reproduction is critically dependent on the trophoblast cell lineage, which assures proper establishment of maternal-fetal interactions during pregnancy. Specification of trophoblast cell lineage begins with the development of the trophectoderm (TE) in preimplantation embryos. Subsequently, other trophoblast cell types arise with progression of pregnancy. Studies with transgenic animal models as well as trophoblast stem/progenitor cells have implicated distinct transcriptional and epigenetic regulators in trophoblast lineage development. This review focuses on our current understanding of transcriptional and epigenetic mechanisms regulating specification, determination, maintenance and differentiation of trophoblast cells.

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Section: Chromatin Remodeling Factors and Trophoblast Developmentmentioning

confidence: 99%

Transcriptional regulators of the trophoblast lineage in mammals with hemochorial placentation

Knott¹,

Paul²

2014

Reproduction

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“…Double-stranded small interfering RNA (siRNA) for SP1 (siSP1) (sc-29487) was purchased with control siRNA (sc-37007) from Santa Cruz Biotechnology. We also established HHUA cells with the stable knockdown of BHLHE40 and BHLHE41 by a lentivirus system (36). The transduced cells were selected by puromycin.…”

Section: Methodsmentioning

confidence: 99%

“…An electrophoretic mobility shift assay (EMSA) was performed using nuclear extracts from 293T cells expressing HA-BHLHE40 and/or FLAG-BHLHE41 as described elsewhere (36). The sequences of the probes used are as follows: pTWIST1-wtSP1BS, 5=-CCGTCCCCTCCCC CTCCCGCCTCCCTCCCCGCCTCCCC-3=; pTWIST1-mtSP1BS, 5=-CC GTCCACTACACATCACGCATACATACACGACTCCCC-3=.…”

Section: Methodsmentioning

confidence: 99%

“…A chromatin immunoprecipitation assay was performed as described elsewhere (36). The DNAprotein complex was immunoprecipitated using anti-SP1 (PEP-2; Santa Cruz Biotechnology), -acetylated histone H3 (Millipore), -HDAC1 (ab7028; Abcam), and -KAT2B (ab12188; Abcam) antibodies and protein G PLUS-agarose (sc-2002; Santa Cruz Biotechnology).…”

Section: Methodsmentioning

confidence: 99%

“…Lentivirus vectors were produced as described previously (36). In order to construct stable cell lines, puromycin and blasticidin were used for pLX302 and pLX303, respectively.…”

Section: Methodsmentioning

confidence: 99%

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Regulation of the Mechanism of TWIST1 Transcription by BHLHE40 and BHLHE41 in Cancer Cells

Asanoma

Liu

Yamane

et al. 2015

Molecular and Cellular Biology

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c BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors that play key roles in multiple cell behaviors. BHLHE40/41 were recently shown to be involved in an epithelial-to-mesenchymal transition (EMT). However, the precise mechanism of EMT control by BHLHE40/41 remains unclear. In the present study, we demonstrated that BHLHE40/41 expression was controlled in a pathological stage-dependent manner in human endometrial cancer (HEC). Our in vitro assays showed that BHLHE40/41 suppressed tumor cell invasion. BHLHE40/41 also suppressed the transcription of the EMT effectors SNAI1, SNAI2, and TWIST1. We identified the critical promoter regions of TWIST1 for its basal transcriptional activity. We elucidated that the transcription factor SP1 was involved in the basal transcriptional activity of TWIST1 and that BHLHE40/41 competed with SP1 for DNA binding to regulate gene transcription. This study is the first to report the detailed functions of BHLHE40 and BHLHE41 in the suppression of EMT effectors in vitro. Our results suggest that BHLHE40/41 suppress tumor cell invasion by inhibiting EMT in tumor cells. We propose that BHLHE40/41 are promising markers to predict the aggressiveness of each HEC case and that molecular targeting strategies involving BHLHE40/41 and SP1 may effectively regulate HEC progression. Basic helix-loop-helix (bHLH) type transcription factors play key roles in cell differentiation, proliferation, apoptosis, and metabolism. BHLHE40 (basic helix-loop-helix family member e40 gene) and BHLHE41 are members of the Hairy/E(spl)/HES family. BHLHE40 and BHLHE41 (BHLHE40/41) exhibit more than 90% similarity in the bHLH region and approximately 50% in total. BHLHE40/41 have been shown to function as transcriptional repressors by binding to the class B E-box. BHLHE40/41 interact with TF2B, TBP, or TF2D or recruit a histone deacetylase at the E-box site (1-5). On the other hand, BHLHE40/41 were previously reported to modulate the expression of some genes in an E-box-independent manner. BHLHE40 has been shown to associate with SP1 binding sites in the BIRC5 promoter to activate its transcription (6) and with STAT3 to regulate the transcription of STAT3-dependent target genes (7). BHLHE41 suppressed VEGF transcription by interacting with HIF1A (8). BHLHE40 and BHLHE41 were reported to associate with retinoid X receptor (RXR), MYOD1, or CEBP in order to regulate the transcription of their target genes (9-12).In diverse types of cancer species, such as colon, oral, and liver cancer or brain tumors, BHLHE40 expression levels were found to be higher in tumors than in adjacent normal tissues (13-15). On the other hand, in human endometrial cancer (HEC) and nonsmall-cell lung cancer, no changes in BHLHE40 expression were reported between cancer and normal tissues (16,17). Regarding expression profiles with the development of cancer, studies on oral, lung, liver, and esophageal cancer showed that BHLHE40 expression inversely correlated with the tumor stage or differentiation grade (18-21)...

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Mutation of the BiP/GRP78 gene causes axon outgrowth and fasciculation defects in the thalamocortical connections of the mammalian forebrain

Favero

Henshaw

Grimsley-Myers

et al. 2012

J of Comparative Neurology

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Proper development of axonal connections is essential for brain function. A forward genetic screen for mice with defects in thalamocortical development previously isolated a mutant called baffled. Here we describe the axonal defects of baffled in further detail and identify a point mutation in the Hspa5 gene, encoding the endoplasmic reticulum chaperone BiP/GRP78. This hypomorphic mutation of BiP disrupts proper development of the thalamocortical axon projection and other forebrain axon tracts, as well as cortical lamination. In baffled mutant brains, a reduced number of thalamic axons innervate the cortex by the time of birth. Thalamocortical and corticothalamic axons are delayed, overfasciculated, and disorganized along their pathway through the ventral telencephalon. Furthermore, dissociated mutant neurons show reduced axon extension in vitro. Together, these findings demonstrate a sensitive requirement for the ER chaperone BiP/GRP78 during axon outgrowth and pathfinding in the developing mammalian brain.

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SATB Homeobox Proteins Regulate Trophoblast Stem Cell Renewal and Differentiation

Cited by 50 publications

References 69 publications

Transcriptional regulators of the trophoblast lineage in mammals with hemochorial placentation

Transcriptional regulators of the trophoblast lineage in mammals with hemochorial placentation

Regulation of the Mechanism of TWIST1 Transcription by BHLHE40 and BHLHE41 in Cancer Cells

Mutation of the BiP/GRP78 gene causes axon outgrowth and fasciculation defects in the thalamocortical connections of the mammalian forebrain

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