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  • 1
    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; INHIBITOR ; carcinoma ; CELL ; Germany ; INHIBITION ; THERAPY ; LUNG-CANCER ; GENE ; PROTEIN ; SAMPLE ; SAMPLES ; TISSUE ; kidney ; FAMILY ; tumour ; ALPHA ; TARGET ; ISOFORM ; immunohistochemistry ; DIFFERENCE ; resistance ; CANCER-CELLS ; BETA ; STRATEGIES ; IMMUNOTHERAPY ; NORMAL TISSUE ; sensitivity ; OVEREXPRESSION ; CANCER-THERAPY ; protein expression ; TRANSCRIPTS ; CELL CARCINOMA ; renal cell carcinoma ; ONCOLOGY ; ADULT ; RE ; THERAPIES ; INCREASE ; cancer therapy ; REAL-TIME ; SURVIVIN ; NUCLEAR ; ML-IAP ; inhibitor of apoptosis ; apoptotic ; quantitative ; livin/ML-IAP ; APOPTOSIS PROTEIN ; CYTOPLASM ; tumour therapy ; Livin/ML-IAP/KIAP ; MELANOMA INHIBITOR
    Abstract: The antiapoptotic Livin/ML-IAP gene has recently gained much attention as a potential new target for cancer therapy. Reports indicating that livin is expressed almost exclusively in tumours, but not in the corresponding normal tissue, suggested that the targeted inhibition of livin may present a novel tumour-specific therapeutic strategy. Here, we compared the expression of livin in renal cell carcinoma and in non-tumorous adult kidney tissue by quantitative real-time reverse transcription-PCR, immunoblotting, and immunohistochemistry. We found that livin expression was significantly increased in tumours (P=0.0077), but was also clearly detectable in non-tumorous adult kidney. Transcripts encoding Livin isoforms alpha and beta were found in both renal cell carcinoma and normal tissue, without obvious qualitative differences. Livin protein in renal cell carcinoma samples exhibited cytoplasmic and/or nuclear staining. In non-tumorous kidney tissue, Livin protein expression was only detectable in specific cell types and restricted to the cytoplasm. Thus, whereas the relative overexpression of livin in renal cell carcinoma indicates that it may still represent a therapeutic target to increase the apoptotic sensitivity of kidney cancer cells, this strategy is likely to be not tumour-specific
    Type of Publication: Journal article published
    PubMed ID: 17968430
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  • 2
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; human ; INHIBITION ; GENE ; PROTEIN ; TISSUE ; CARCINOGENESIS ; DOWN-REGULATION ; E7 ; papillomavirus ; TARGET ; virus ; ELEMENT ; LESIONS ; PROMOTER ; cervical cancer ; CERVICAL-CANCER ; p53 ; GROWTH-INHIBITION ; human papillomavirus ; CANCER-CELLS ; HPV ; E6 ; ONCOGENE ; HPV16 ; HUMAN-PAPILLOMAVIRUS ; CARCINOMAS ; POSITIVE CANCER-CELLS ; TRANSLOCATION ; OVEREXPRESSION ; REPRESSION ; RETINOIC ACID ; E6 ONCOPROTEIN ; TUMOR-SUPPRESSOR ; papillomaviruses ; LEVEL ; tumor suppressor gene ; EPITHELIUM ; USA ; oncogenes ; B-CELL ; HUMAN PAPILLOMAVIRUSES ; tumor suppressor genes ; NOV ; tumor suppressor ; Luciferase reporter ; BTG2 ; cervical cancers ; viral carcinogenesis
    Abstract: Human papillomavirus (HPV)-induced carcinogenesis is critically dependent on the activities of the viral E6 and E7 oncogenes. Here, we demonstrate that expression of the putative tumor suppressor gene B-cell translocation gene-2 (BTG2) is reinduced in HPV16- and HPV18-positive cancer cells on silencing of viral oncogene expression, indicating that BTG2 is repressed by oncogenic HPVs. Inhibition of BTG2 expression was mediated by the HPV E6 oncogene and occurred in a p53-dependent manner. Luciferase reporter gene analyses revealed that BTG2 repression takes place at the transcriptional level and is dependent on the integrity of the major p53-response element within the BTG2 promoter. Ectopic expression of BTG2 acted antiproliferative in cervical cancer cells. Tissue specimens commonly exhibited reduced BTG2 protein levels in HPV-positive high-grade lesions (CIN2/3) and cervical carcinomas, when compared with normal cervical epithelium. These findings identify the antiproliferative BTG2 gene as a novel cellular target blocked by the HPV E6 oncoprotein. (C) 2009 UICC
    Type of Publication: Journal article published
    PubMed ID: 19551855
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  • 3
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; proliferation ; tumor ; TUMOR-CELLS ; CELL ; CELL-PROLIFERATION ; Germany ; human ; IN-VIVO ; VIVO ; GENE ; GENES ; PROTEIN ; PROTEINS ; RNA ; RELEASE ; ACTIVATION ; cell cycle ; CELL-CYCLE ; E7 ; papillomavirus ; BREAST-CANCER ; TARGET ; virus ; LESIONS ; PROGRESSION ; resistance ; cervical cancer ; CERVICAL-CANCER ; PROSTATE-CANCER ; human papillomavirus ; TYPE-16 ; CANCER-CELLS ; HPV ; E6 ; ONCOGENE ; HPV16 ; HUMAN-PAPILLOMAVIRUS ; PHENOTYPE ; ONCOPROTEIN ; METHYLTRANSFERASE ACTIVITY ; E6 ONCOPROTEIN ; ONCOLOGY ; ENHANCER ; RE ; INTERFERENCE ; RNA INTERFERENCE ; LEVEL ; USA ; oncogenes ; cancer research ; viral ; transformed cell ; GROUP PROTEIN EZH2 ; POLYCOMB REPRESSION
    Abstract: The malignant phenotype of human papillomavirus (HPV)-positive cancer cells is maintained by the activity of the viral E6 and E7 genes. Here, we identified the polycomb group gene enhancer of zeste homologue 2 (EZH2) as a novel downstream target for the viral oncogenes in HPV transformed cells. EZH2 expression was activated by HPV16 E7 at the transcriptional level via E7-mediated release of E2F from pocket proteins. RNA interference analyses showed that continuous EZH2 expression is required for the proliferation of HPV-positive tumor cells by stimulating cell cycle progression at the G(1)-S boundary. In addition to its growth-promoting activity, EZH2 also contributed to the apoptotic resistance of cervical cancer cells. Furthermore, we found that HPV-positive dysplastic and tumorigenic cervical lesions were characterized by high levels of EZH2 protein in vivo. We conclude that the E7 target gene EZH2 is a major determinant for the proliferation of HPV-positive cancer cells and contributes to their apoptotic resistance. Moreover, EZH2 may serve as a novel therapeutic target for the treatment of cervical cancer. [Cancer Res 2008;68(23):9964-72]
    Type of Publication: Journal article published
    PubMed ID: 19047178
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  • 4
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; proliferation ; tumor ; carcinoma ; CELL ; CELL-PROLIFERATION ; Germany ; human ; INHIBITION ; THERAPY ; HEPATOCELLULAR-CARCINOMA ; GENE ; RNA ; SAMPLE ; SAMPLES ; TISSUE ; LINES ; kidney ; primary ; CELL-LINES ; TARGET ; virus ; MALIGNANCIES ; resistance ; CARCINOMA CELLS ; PROSTATE-CANCER ; CELL-LINE ; CARCINOMA-CELLS ; HOMOLOG ; STRATEGIES ; METHYLTRANSFERASE ACTIVITY ; CANCER-THERAPY ; CELL CARCINOMA ; renal cell carcinoma ; MALIGNANCY ; ONCOLOGY ; ENHANCER ; ADULT ; RE ; INTERFERENCE ; RNA INTERFERENCE ; THERAPIES ; cancer therapy ; cell proliferation ; TUMOR TISSUE ; LEVEL ; RNAi ; USA ; tumor therapy ; RENAL-CELL ; GROUP PROTEIN EZH2 ; POLYCOMB REPRESSION ; HISTONE H3 ; AGGRESSIVE BREAST-CANCER ; enhancer of zeste homolog 2 (EZH2) ; ZESTE HOMOLOG-2
    Abstract: The enhancer of zeste homolog 2 (EZH2) gene has been recently linked to human malignancies where it may serve as a new target for cancer therapy. Here, we analyzed EZH2 expression in primary renal cell carcinoma (RCC) specimens and in nontumorous tissue samples from adult kidney. EZH2 transcripts were detectable in all RCC specimens examined. Expression levels were significantly higher in tumor tissue (p 〈= 0.0001) than in samples from normal adult kidney. Moreover, inhibition of endogenous EZH2 expression in RCC cell lines by RNA interference (RNAi) led to reduced proliferation and increased apoptosis in RCC cells. These data show that EZH2 is overexpressed in RCC. Furthermore, they indicate that the EZH2 gene plays a role for both the proliferation and the apoptosis resistance of RCC cells. Targeted inhibition of EZH2 could therefore represent a novel strategy to improve the therapeutic response of RCC. (C) 2008 Wilely-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18623083
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  • 5
    Keywords: CELLS ; EXPRESSION ; GROWTH ; proliferation ; CELL ; Germany ; INHIBITION ; GENE ; PROTEIN ; MECHANISM ; TRANSPLANTATION ; mechanisms ; cell cycle ; CYCLE ; papillomavirus ; PHOSPHORYLATION ; p53 ; human papillomavirus ; CANCER-CELLS ; ANTIVIRAL ACTIVITY ; NEPHROPATHY ; P53 GENE MUTATION ; cell proliferation ; HUMAN PAPILLOMAVIRUSES ; cytomegalovirus ; TACROLIMUS ; MEDIATOR ; FK778 ; IMMUNOSUPPRESSIVE AGENT LEFLUNOMIDE ; malononitrilamides
    Abstract: The malononitrilamide FK778 is a novel immunosuppressive agent with antiproliferative activities. To gain insight into the molecular mechanism of FK778-mediated growth inhibition, we analyzed cells which differ in their p53 status and functionality of retinoblastoma protein (pRb). FK778 acted as a broad inhibitor of cell proliferation independent of the p53 or pRb status. However, the mechanism of FK778-mediated growth inhibition differed, leading either to cell cycle arrest in G1, or cell accumulation in S phase. This differential response was linked to the phosphorylation status of pRb. In addition, since FK778 was reported to exhibit antiviral activities, we analyzed the effect of FK778 on the growth Stimulatory human papillomavirus (HPV)-16 and -18 E7 genes. Although growth of HPV-positive cells was strongly inhibited by FK778, we did not observe significant effects on viral E7 expression, indicating that the antiproliferative effect is not linked to an antiviral activity of FK778
    Type of Publication: Journal article published
    PubMed ID: 19212661
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  • 6
    Keywords: CANCER ; EXPRESSION ; proliferation ; SURVIVAL ; carcinoma ; DISEASE ; GENE ; microarray ; MARKER ; BREAST ; DOUBLE-BLIND ; CELL CARCINOMA ; PREDICT ; PHASE-III TRIAL ; GROUP PROTEIN EZH2 ; ENHANCER-OF-ZESTE-HOMOLOG-2 GENE ; METASTATIC PROSTATE-CANCER
    Abstract: Background: The enhancer of zeste homolog 2 (EZH2) gene exerts oncogene-like activities and its (over) expression has been linked to several human malignancies. Here, we studied a possible association between EZH2 expression and prognosis in patients with renal cell carcinoma (RCC). Methods: EZH2 protein expression in RCC specimens was analyzed by immunohistochemistry using a tissue microarray (TMA) containing RCC tumor tissue and corresponding normal tissue samples of 520 patients. For immunohistochemical assessment of EZH2 expression, nuclear staining quantity was evaluated using a semiquantitative score. The effect of EZH2 expression on cancer specific survival (CSS) was assessed by univariate and multivariate Cox regression analyses. Results: During follow-up, 147 patients (28%) had died of their disease, median follow-up of patients still alive was 6.0 years (range 0-16.1 years). EZH2 nuclear staining was present in tumor cores of 411 (79%) patients. A multivariate Cox regression analysis revealed that high nuclear EZH2 expression was an independent predictor of poor CSS (〉 25-50% vs. 0%: HR 2.72, p = 0.025) in patients suffering from non-metastatic RCC. Apart from high nuclear EZH2 expression, tumor stage and Fuhrman's grading emerged as significant prognostic markers. In metastatic disease, nuclear EZH2 expression and histopathological subtype were independent predictive parameters of poor CSS (EZH2: 1-5%: HR 2.63, p = 0.043, 〉 5-25%: HR 3.35, p = 0.013, 〉 25%-50%: HR 4.92, p = 0.003, all compared to 0%: HR 0.36, p = 0.025, respectively). Conclusions: This study defines EZH2 as a powerful independent unfavourable prognostic marker of CSS in patients with metastatic and non-metastatic RCC
    Type of Publication: Journal article published
    PubMed ID: 20920340
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