Ectopic EBP2 expression enhances cyclin E1 expression and induces chromosome instability in HEK293 stable clones

Lee, Ming‐Cheng; Hsieh, Chang‐Hsun; Wei, Shu–Chen; Shen, S. C.; Chen, Chiung-Nien; Wu, Vin‐Cent; Chuang, Li-Ying; Hsieh, Fon‐Jou; Wu, Chaowei; Tsai-Wu, Jyy-Jih

doi:10.5483/bmbrep.2008.41.10.716

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…Although previous study indicates that overexpression of EBP2 can promote the cell proliferation of HEK293 cells, 21 its role in the tumorigenesis is still unclear. In our study, we identified that EBP2 is upregulated in lung cancer cells and tissues.…”

Section: Discussionmentioning

confidence: 96%

“…20 Overexpression of EBP2 has been shown to be able to promote the cell proliferation and chromosome instability of 293 cells or NIH3T3 cells. 21, 22 A recent study demonstrates that EBP2 is essential for the nucleolar localization of Fbw7γ via direction interaction. 23 However, the biological functions of mammal EBP2, such as whether it may affect the stability of Fbw7 γ substrates, remain not completely understood.…”

mentioning

confidence: 99%

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A positive feedback loop between EBP2 and c-Myc regulates rDNA transcription, cell proliferation, and tumorigenesis

et al. 2014

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The oncoprotein c-Myc is a key transcription factor with essential functions in the nucleolus (NO) to regulate ribosomal RNA (rRNA) synthesis, ribosome biogenesis, and cell proliferation. Yet, the mechanism that regulates the distribution and function of nucleolar c-Myc is still not completely understood. In this study, we identified nucleolar protein ENBA1 binding protein 2 (EBP2) as a novel functional binding partner of c-Myc. We found that coexpression of EBP2 markedly relocalized c-Myc from the nucleus to the NO, whereas depletion of EBP2 reduced the nucleolar distribution of c-Myc. Further study indicated that EBP2 is a direct binding partner of c-Myc and can block the degradation of c-Myc in a FBW7 (F-box and WD repeat domain containing 7)-independent manner. Moreover, EBP2 is a transcriptional target of c-Myc. c-Myc can bind to the promoter of EBP2 and positively regulate the EBP2 expression. Both protein and mRNA levels of EBP2 are upregulated in lung cancer samples and positively correlated with c-Myc expression. Functionally, EBP2 promotes c-Myc-mediated rRNA synthesis and cell proliferation. Collectively, our study indicates that EBP2 is a novel binding partner of c-Myc that regulates the function of nucleolar c-Myc, cell proliferation, and tumorigenesis via a positive feedback loop.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

A positive feedback loop between EBP2 and c-Myc regulates rDNA transcription, cell proliferation, and tumorigenesis

et al. 2014

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“…of cyclin E1 and subsequent chromosome instability (26,33). Whether EBNA-1 modulates such aspect of EBP2 functions during interphase merits a careful examination.…”

Section: Discussionmentioning

confidence: 99%

Live-Cell Imaging Reveals Multiple Interactions between Epstein-Barr Virus Nuclear Antigen 1 and Cellular Chromatin during Interphase and Mitosis

Jourdan

Jobart-Malfait

Reis

et al. 2012

J Virol

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e Epstein-Barr virus (EBV) establishes a life-long latent infection in humans. In proliferating latently infected cells, EBV genomes persist as multiple episomes that undergo one DNA replication event per cell cycle and remain attached to the mitotic chromosomes. EBV nuclear antigen 1 (EBNA-1) binding to the episome and cellular genome is essential to ensure proper episome replication and segregation. However, the nature and regulation of EBNA-1 interaction with chromatin has not been clearly elucidated. This activity has been suggested to involve EBNA-1 binding to DNA, duplex RNA, and/or proteins. EBNA-1 binding protein 2 (EBP2), a nucleolar protein, has been proposed to act as a docking protein for EBNA-1 on mitotic chromosomes. However, there is no direct evidence thus far for EBP2 being associated with EBNA-1 during mitosis. By combining video microscopy and Förster resonance energy transfer (FRET) microscopy, we demonstrate here for the first time that EBNA-1 and EBP2 interact in the nucleoplasm, as well as in the nucleoli during interphase. However, in strong contrast to the current proposed model, we were unable to observe any interaction between EBNA-1 and EBP2 on mitotic chromosomes. We also performed a yeast doublehybrid screening, followed by a FRET analysis, that led us to identify HMGB2 (high-mobility group box 2), a well-known chromatin component, as a new partner for EBNA-1 on chromatin during interphase and mitosis. Although the depletion of HMGB2 partly altered EBNA-1 association with chromatin in HeLa cells during interphase and mitosis, it did not significantly impact the maintenance of EBV episomes in Raji cells.

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“…Karyotype analysis of 293_CHI3L1 clones have shown that these cells differ from wild type [31,32] and control cells (293_pcDNA3.1) in modal chromosome number and structure of chromosomes (manuscript in preparation). Other authors have also shown that overexpression, for example, of tripeptidyl-peptidase II [33], EBNA1 binding protein 2 [34], GLI1 transcripton factor [35] or Cut homeobox 1 trancription factor [36] have triggered centrosome and chromosomal abnormalities in 293 cells.…”

Section: Immortalization and Transformation: The Central Role Of Karymentioning

confidence: 99%

Cancer Genes and Chromosome Instability

Stepanenko¹,

Kavsan²

2013

Oncogene and Cancer - From Bench to Clinic

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Ectopic EBP2 expression enhances cyclin E1 expression and induces chromosome instability in HEK293 stable clones

Cited by 4 publications

References 26 publications

A positive feedback loop between EBP2 and c-Myc regulates rDNA transcription, cell proliferation, and tumorigenesis

A positive feedback loop between EBP2 and c-Myc regulates rDNA transcription, cell proliferation, and tumorigenesis

Live-Cell Imaging Reveals Multiple Interactions between Epstein-Barr Virus Nuclear Antigen 1 and Cellular Chromatin during Interphase and Mitosis

Cancer Genes and Chromosome Instability

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