Transcriptional regulation of OCT4 by the ETS transcription factor ESE-1 in NCCIT human embryonic carcinoma cells

Park, Sung-Won; Do, Hyun-Jin; Ha, Woo Tae; Han, Mi-Hee; Yang, Hyun Ok; Lee, Soo−Hong; Song, Hyuk; Kim, Nam‐Hyung; Kim, Jaehwan

doi:10.1016/j.bbrc.2014.06.079

Cited by 8 publications

(6 citation statements)

References 38 publications

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“…By examining significant global transcriptional changes (p < 0.05, fold change ≥ 1.5) immediately preceding the onset of reprogramming, we identified 320 up-regulated and 337 down-regulated genes in Nanog + Sin3a pre-iPSCs relative to Nanog + EV pre-iPSCs (Figure 4A). We identified up-regulated genes implicated in pluripotency and reprogramming including Cited2 (Kranc et al, 2015), Elf3 (Park et al, 2014), Klf1 (Nakagawa et al, 2008), Nfya (Dolfini et al, 2012), and Trp53bp1 (Marión et al, 2009) (Figure 4A, red text), and also identified several down-regulated genes known to act as barriers during the reprogramming process (Qin et al, 2014; Sakurai et al, 2014; Yang et al, 2014) (Figure 4A, blue text). We further validated the differential expression of a number of these reprogramming promoting and barrier genes by qRT-PCR (Figure S4A).…”

Section: Resultsmentioning

confidence: 99%

The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency

et al. 2017

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SUMMARY Although Sin3a is required for survival of early embryos and embryonic stem cells (ESCs), the role of Sin3a in the maintenance and establishment of pluripotency remains unclear. Here we find that the Sin3a/HDAC corepressor complex maintains ESC pluripotency and promotes the generation of induced pluripotent stem cells (iPSCs). Members of the Sin3a/HDAC corepressor complex are enriched in an extended Nanog interactome and function in transcriptional coactivation in ESCs. We also identified a critical role for Sin3a and HDAC2 in efficient reprogramming of somatic cells. Mechanistically, Nanog and Sin3a co-occupy transcriptionally active pluripotency genes in ESCs and also co-localize extensively at their genome-wide targets in pre-iPSCs. Additionally, both factors are required to directly induce a synergistic transcriptional program wherein pluripotency genes are activated and reprogramming barrier genes are repressed. Our findings indicate a transcriptional regulatory role for a major HDAC-containing complex in promoting pluripotency.

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Section: Resultsmentioning

confidence: 99%

The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency

et al. 2017

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“…38) We also previously reported that OCT4 and GDF3 are highly expressed in pluripotent human EC NCCIT cells and that this expression is reduced upon RA treatment in a time-dependent manner. 30,36,37,39,40) However, there is no report concerning the interaction between OCT4 and GDF3 at the transcriptional level. Therefore, to investigate their transcriptional relationship in pluripotent germ cell-derived EC cells, we first examined the expression of GDF3 and OCT4 in NCCIT cells during RA-mediated differentiation.…”

Section: Resultsmentioning

confidence: 99%

“…34,35) Western Blot Analysis NCCIT cells were treated with RA for different amounts of time (0, 2, 4, 6, 8, 10 d) and harvested, or transfected with OCT4-targeting shRNA or the Flag-tagged OCT4 expression vector using the ViaFect transfection reagent (Promega) and harvested 48 h later. Western blotting was performed as previously described 36,37) with a minor modification. Membranes were blocked in 1% bovine serum albumin and incubated with anti-OCT4 polyclonal Each primary antibody-complexed membrane was further incubated with a horseradish peroxidase-conjugated secondary antibody (1 : 5000, Santa Cruz Biotechnology).…”

Section: )mentioning

confidence: 99%

Growth and Differentiation Factor 3 Is Transcriptionally Regulated by OCT4 in Human Embryonic Carcinoma Cells

Han

Park

et al. 2016

Biological & Pharmaceutical Bulletin

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Growth and differentiation factor 3 (GDF3), a mammalian-specific transforming growth factor β ligand, and OCT4, one of key stem cell transcription factors, are expressed in testicular germ cell tumors (TGCTs) as well as pluripotent stem cells. To understand the molecular mechanism by which OCT4 and GDF3 function in tumorigenesis as well as stemness, we investigated the transcriptional regulation of GDF3 mediated by OCT4 in human embryonic carcinoma (EC) NCCIT cells, which are pluripotent stem cells of TGCTs. GDF3 and OCT4 was highly expressed in undifferentiated NCCIT cells and then significantly decreased upon retinoic acid-induced differentiation in a time-dependent manner. Moreover, GDF3 expression was reduced by short hairpin RNA-mediated knockdown of OCT4 and increased by OCT4 overexpression, suggesting that GDF3 and OCT4 have a functional relationship in pluripotent stem cells. A promoter-reporter assay revealed that the GDF3 promoter ( 1721-Luc) activity was significantly activated by OCT4 in a dose-dependent manner. Moreover, the minimal promoter ( 183-Luc) was sufficient for OCT4-mediated transcriptional activation and provided a potential binding site for the direct interaction with OCT4. Collectively, this study provides the evidence about the regulatory mechanism of GDF3 mediated by OCT4 in pluripotent EC cells.

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“…One of the targets is MMP-9 which was downregulated by ESE-1 through ETS-binding site on the MMP-9 promoter in squamous cell carcinoma (11). ESE-1 downregulates OCT4, a transcription factor, involved in stem cell pluripotency of NCCIT human embryonic carcinoma cells (27). Another interesting target gene we propose is wnt/β-catenin as we previously observed that ESE-1 physically interacts with β-catenin (20) and suppresses transcriptional activity of β-catenin/LEF (data not shown).…”

Section: Discussionmentioning

confidence: 99%

ESE‑1 suppresses the growth, invasion and migration of human NSCLC cells and tumor formation in�vivo

Lou

Lee

et al. 2018

Oncol Rep

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Lung cancer is the first leading cause of cancer‑related death in the United States. Non‑small cell lung cancer (NSCLC) is the most common type of lung cancer and is associated with a poor patient prognosis. Identification of promising molecular targets is required for the effective prevention and therapy of NSCLC. Epithelial‑specific ETS‑1 (ESE‑1) belongs to the superfamily of ETS transcription factors. The effect of ESE‑1 on tumorigenesis is controversial in several types of cancer while its role in lung cancer remains unknown. The present study was designed to investigate whether ESE‑1 expression affects tumorigenic activity using human NSCLC cells and a mouse xenograft model. ESE‑1 expression suppressed anchorage‑independent growth in soft agar assay and led to an increase in G1 arrest and apoptosis in human NSCLC cells. ESE‑1 expression suppressed the invasion and migration of human NSCLC cells. Western blot analysis, RT‑PCR and promoter assay indicated that ESE‑1 expression was transcriptionally downregulated by treatment of transforming growth factor (TGF)‑β, an EMT (epithelial‑mesenchymal transition) stimulator. The xenograft study indicated that ESE‑1 expression inhibited tumor formation and development. Our data demonstrated that ESE‑1 plays a key role as a tumor suppressor in human NSCLC.

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Transcriptional regulation of OCT4 by the ETS transcription factor ESE-1 in NCCIT human embryonic carcinoma cells

Cited by 8 publications

References 38 publications

The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency

The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency

Growth and Differentiation Factor 3 Is Transcriptionally Regulated by OCT4 in Human Embryonic Carcinoma Cells

ESE‑1 suppresses the growth, invasion and migration of human NSCLC cells and tumor formation in�vivo

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