Customized rapid subtraction hybridization (RaSH) gene microarrays identify overlapping expression changes in human fetal astrocytes resulting from human immunodeficiency virus-1 infection or tumor necrosis factor-α treatment

Su, Zao-zhong; Chen, Yinming; Kang, Dong‐Chul; Chao, Wei; Simm, Malgorzata; Volsky, David J.; Fisher, Paul B.

doi:10.1016/s0378-1119(03)00404-9

Cited by 74 publications

(73 citation statements)

References 44 publications

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“…AEG-1 is overexpressed in multiple cancers and it cooperates with ras to promote transformation of melanocytes (3). AEG-1 is also induced by TNF-a treatment (2). In these contexts, we hypothesized that AEG-1 might activate the NF-nB pathway, a known TNF-a-induced signaling cascade that is activated in multiple tumors.…”

Section: Adaeg-1 Infection Generates Aeg-1 Proteinmentioning

confidence: 99%

“…We recently reported the full-length cloning and functional characterization of an HIV-1-inducible gene, astrocyte elevated gene-1 (AEG-1), which displays slow induction kinetics following HIV infection or gp120 treatment (1)(2)(3). AEG-1 mRNA is expressed ubiquitously with higher expression in tissues containing muscular actin and its expression is increased in astrocytes infected with HIV-1 or treated with gp120 or tumor necrosis factor a (TNF-a; ref.…”

Section: Introductionmentioning

confidence: 99%

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Activation of the Nuclear Factor κB Pathway by Astrocyte Elevated Gene-1: Implications for Tumor Progression and Metastasis

Emdad¹,

Sarkar²,

Su³

et al. 2006

Cancer Research

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258

355

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Astrocyte elevated gene-1 (AEG-1) was initially identified as an HIV-1-and tumor necrosis factor A (TNF-A)-inducible transcript in primary human fetal astrocytes by a rapid subtraction hybridization approach. Interestingly, AEG-1 expression is elevated in subsets of breast cancer, glioblastoma multiforme and melanoma cells and AEG-1 cooperates with Ha-ras to promote transformation of immortalized melanocytes. Activation of the transcription factor nuclear factor KB (NF-KB), a TNF-A downstream signaling component, is associated with several human illnesses, including cancer, and NF-KB controls the expression of multiple genes involved in tumor progression and metastasis. We now document that AEG-1 is a significant positive regulator of NF-KB. Enhanced expression of AEG-1 via a replication-incompetent adenovirus (Ad.AEG-1) in HeLa cells markedly increased binding of the transcriptional activator p50/p65 complex of NF-KB. The NF-KB activation induced by AEG-1 corresponded with degradation of IKBA and nuclear translocation of p65 that resulted in the induction of NF-KB downstream genes. Infection with an adenovirus expressing the mt32IKBA superrepressor (Ad.IKBA-mt32), which prevents p65 nuclear translocation, inhibited AEG-1-induced enhanced agar cloning efficiency and increased matrigel invasion of HeLa cells. We also document that TNF-A treatment resulted in nuclear translocation of both AEG-1 and p65 wherein these two proteins physically interacted, suggesting a potential mechanism by which AEG-1 could activate NF-KB. Our findings suggest that activation of NF-KB by AEG-1 could represent a key molecular mechanism by which AEG-1 promotes anchorage-independent growth and invasion, two central features of the neoplastic phenotype.

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Section: Adaeg-1 Infection Generates Aeg-1 Proteinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activation of the Nuclear Factor κB Pathway by Astrocyte Elevated Gene-1: Implications for Tumor Progression and Metastasis

Emdad¹,

Sarkar²,

Su³

et al. 2006

Cancer Research

Self Cite

258

355

View full text Add to dashboard Cite

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“…Primary human fetal astrocyte cells were generated from human fetal brain tissue obtained from the products of elective abortions in full compliance with NIH guidelines, and were kindly provided by Dr Volsky and colleagues (Su et al, 2002(Su et al, , 2003. PHFA, IM-PHFA, FM516 and FM516-ras cells were cultured as described .…”

Section: Cell Cultures and Reagentsmentioning

confidence: 99%

“…Astrocyte elevated gene-1 (AEG-1) was cloned in our laboratory as a novel gene with elevated expression in primary human fetal astrocytes (PHFA) infected with human immunodeficiency virus type 1 (HIV-1) or treated with gp120 or tumor necrosis factor a (TNF-a) (Su et al, 2002(Su et al, , 2003. Intriguingly, AEG-1 is highly expressed in subsets of breast carcinomas, malignant gliomas and melanomas, and it synergizes with oncogenic Ha-ras to enhance soft agar colony formation of nontumorigenic immortalized melanocytes .…”

Section: Introductionmentioning

confidence: 99%

Astrocyte elevated gene-1 activates cell survival pathways through PI3K-Akt signaling

et al. 2007

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“…Moreover, inhibition of EGFR with cetuximab plus radiotherapy increased overall survival when compared with the use of radiotherapy alone (10). Metadherin (MTDH, also known as AEG-1) was originally reported as a protein induced in primary human fetal astrocytes infected with HIV-1 or treated with either HIV gp120 or TNF-α (11,12). MTDH synergizes with oncogenic Ha-ras to enhance the softagar-colony-forming ability of non-tumorigenic immortalized melanocytes (13).…”

Section: Introductionmentioning

confidence: 99%

Metadherin regulates radioresistance in cervical cancer cells

et al. 2012

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Abstract. Metadherin (MTDH) promotes cancer metastasis, chemoresistance, invasion and angiogenesis. Upregulation of MTDH is correlated with both progression and poor clinical outcome of many types of cancers; however, there is currently no information regarding the role of MTDH in radiation sensitivity. Here, we investigated the effects of MTDH on the radiosensitivity of cervical cancer cells using the SiHa cell line. We discovered that cervical cancer cells in which MTDH was knocked down had significantly increased radiosensitivity as measured by a clonogenic assay. MTDH knockdown cells also had increased apoptosis and a decreased proportion of cells arrested in the G2 phase after radiation treatment. MTDH knockdown also weakened the repair of DNA double-strand breaks (DSBs) induced by radiation. These results indicate that MTDH affects the radiosensitivity of cervical cancer cells and that MTDH may be a novel target to improve cervical cancer radiation response.

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Customized rapid subtraction hybridization (RaSH) gene microarrays identify overlapping expression changes in human fetal astrocytes resulting from human immunodeficiency virus-1 infection or tumor necrosis factor-α treatment

Cited by 74 publications

References 44 publications

Activation of the Nuclear Factor κB Pathway by Astrocyte Elevated Gene-1: Implications for Tumor Progression and Metastasis

Activation of the Nuclear Factor κB Pathway by Astrocyte Elevated Gene-1: Implications for Tumor Progression and Metastasis

Astrocyte elevated gene-1 activates cell survival pathways through PI3K-Akt signaling

Metadherin regulates radioresistance in cervical cancer cells

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