Suppression of salivary adenoid cystic carcinoma growth and metastasis by ErbB3 binding protein Ebp1 gene transfer

Yu, Youcheng; Chen, Wantao; Zhang, Yuexing; Hamburger, Anne W.; Pan, Haiyang; Zhang, Zhiyuan

doi:10.1002/ijc.22541

Cited by 30 publications

(49 citation statements)

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“…Cells on the upper surface of the filter were removed by wiping with a cotton swab, and invasion was determined by counting the cells that migrated to the lower side of the filter with optical microscopy at x400 magnification. A total of 5 visual fields at the center and in the surrounding areas was counted, and the average was calculated (22). The experiment was repeated 3 times.…”

Section: Soft Agar Colony Formation Assay Briefly 4x10mentioning

confidence: 99%

ADAM10 is overexpressed in human hepatocellular carcinoma and contributes to the proliferation, invasion and migration of HepG2 cells

Shao

Shi

2013

Oncology Reports

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Abstract.The overexpression of A disintegrin and metalloproteinase 10 (ADAM10) has been found to be closely associated with the development and progression of various types of tumors. However, ADAM10 expression in hepatocellular carcinoma (HCC) and its significance remain largely unknown. The present study aimed to investigate the expression of ADAM10 in human HCC and the effect of ADAM10 gene silencing by siRNA on the proliferation, invasion and migration of HepG2 human hepatoma cells. Immunohistochemistry was performed to examine the expression of ADAM10 in human HCC tissues and in the adjacent non-cancer tissues from 30 patients with HCC. RNA interference was used to knock down ADAM10 expression in HepG2 human hepatoma cells and the proliferation and migration as well as the invasive ability of the treated cells were observed in vitro. The expression of ADAM10 protein in HCC tissues was significantly higher when compared to that in adjacent non-tumor tissues (P<0.05). The high expression of ADAM10 in cancer was significantly correlated with clinical outcomes (P<0.05). Silencing of ADAM10 resulted in inhibition of proliferation and migration as well as invasion of HepG2 human hepatoma cells (P<0.05). These studies suggest that ADAM10 plays an important role in regulating proliferation, invasion and migration of HepG2 cells. High expression of ADAM10 may be a valuable predictive factor for HCC prognosis, and ADAM10 is potentially an important therapeutic target for the prevention of tumor development and progression in HCC.

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Section: Soft Agar Colony Formation Assay Briefly 4x10mentioning

confidence: 99%

ADAM10 is overexpressed in human hepatocellular carcinoma and contributes to the proliferation, invasion and migration of HepG2 cells

Shao

Shi

2013

Oncology Reports

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“…Western blot analysis was performed as previously described (Yu et al 2007;Zhang et al 2002). The Ebp1 antibody is from Oncogene (USA) and the polyclone antibody against actin is from Sigma.…”

Section: Western Blottingmentioning

confidence: 99%

“…Proliferation rates were assessed by measuring the incorporation of 3 H-thymidine into newly replicated DNA as previously described (Yu et al 2007).…”

Section: Proliferation Assaymentioning

confidence: 99%

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Potential therapeutic strategy for oral squamous cell carcinoma by ErbB3-binding protein 1 gene transfer

Zhou

Chen

Zhang

et al. 2009

J Cancer Res Clin Oncol

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“…Ebp1 contains an autonomous C-terminal transcriptional repression domain that binds histone deacetylase 2 (Zhang et al, 2003). It strongly suppresses both androgen receptor-mediated gene transcription and tumorigenesis of prostate cancer cells and salivary adenoid carcinoma cell metastasis in mice (Zhang et al, 2005b;Akinmade et al, 2007;Yu et al, 2007). Collectively, these observations suggest that Ebp1 p42 acts as a potent tumor suppressor in various human cancers, whereas p48 might function as an oncogene, promoting cell survival and proliferation.…”

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confidence: 95%

Human BRE1 Is an E3 Ubiquitin Ligase for Ebp1 Tumor Suppressor

Liu¹,

Oh²,

Okada³

et al. 2009

MBoC

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Human Bre1, an E3 ligase for H2B monoubiquitination, binds p53 and enhances activator-dependent transcription. Ebp1, an ErbB3 receptor-binding protein, inhibits cell proliferation and acts as a tumor suppressor. Here, we show that hBre1 acts as an E3 ubiquitin ligase for Ebp1 tumor suppressor and promotes its polyubiquitination and degradation. Ebp1 is polyubiquitinated in cancer cells, which is regulated by its phosphorylation. We identified hBre1 acting as an E3 ligase for Ebp1 and increasing its polyubiquitination. Depletion of hBre1 blocks Ebp1's polyubiquitination and elevates its protein level, preventing cancer proliferation. hBre1 binds Ebp1 and suppresses its repressive effect on E2F-1. Moreover, Ebp1 protein level is substantially diminished in human cancers. It is robustly phosphorylated and localized in the nucleus of primary gliomas, correlating with hBre1 subcellular residency. Thus, hBre1 inhibits Ebp1's tumor suppressive activity through mediating its polyubiquitination and degradation. INTRODUCTIONIn yeast, histone H2B K123 monoubiquitination is regulated by the E3 ligase Bre1 and E2-conjugating enzyme RAD6 (Robzyk et al., 2000;Hwang et al., 2003;Wood et al., 2003a). This process is a prerequisite for the subsequent histone H3-K4 and K79 methylation (Sun and Allis, 2002;Wood et al., 2003b), which marks actively transcribed genes (SantosRosa et al., 2002). Additionally, PAF complex is also required for H2B ubiquitination (Ng et al., 2003;Wood et al., 2003b). In humans, the homologue of yeast Bre1 (RNF20), designated as hBre1, acts as an E3 ligase for H2B and promotes its ubiquitination at K120, the equivalent of yeast H2B K123 (Kim et al., 2005;Zhu et al., 2005). Moreover, it has a coactivator function in activator-dependent transcription of several genes. Interestingly, hBre1 directly binds p53 and is recruited to the MDM2 promoter, regulating p53-responsive gene transcription in a p53-dependent manner. Overexpression and depletion of hBre1 increases and decreases global H2B ubiquitination, respectively. By contrast, ectopic hRAD6A and hRAD6B, human homologues of yRAD6, do not affect H2B ubiquitination or H3 methylation, suggesting that hRAD6 proteins are not cognate E2 enzymes for hBre1 (Kim et al., 2005). In addition to transcriptional coactivation of specific genes (Osley, 2004), Bre1 in Drosophila is required for Notch signaling and histone modification (Bray et al., 2005).Ebp1 was originally identified as an ErbB3 receptor-binding protein , and it is the human homologue of a previously identified cell cycle-regulated mouse protein p38-2G4 (Radomski and Jost, 1995). PA2G4 gene encodes two Ebp1 isoforms, p48 and p42, which differentially regulate PC12 cell survival and differentiation Liu et al., 2006). P48 is 54 amino acids longer than p42 at its N terminus. The longer form p48 localizes in both the cytoplasm and the nucleolus and suppresses apoptosis, whereas the shorter form p42 predominantly resides in the cytoplasm and promotes cell differentiation . Ebp1 binds the ribosome and double-st...

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Suppression of salivary adenoid cystic carcinoma growth and metastasis by ErbB3 binding protein Ebp1 gene transfer

Cited by 30 publications

References 30 publications

ADAM10 is overexpressed in human hepatocellular carcinoma and contributes to the proliferation, invasion and migration of HepG2 cells

ADAM10 is overexpressed in human hepatocellular carcinoma and contributes to the proliferation, invasion and migration of HepG2 cells

Potential therapeutic strategy for oral squamous cell carcinoma by ErbB3-binding protein 1 gene transfer

Human BRE1 Is an E3 Ubiquitin Ligase for Ebp1 Tumor Suppressor

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