Transcriptional and translational downregulation of H-REV107, a class II tumour suppressor gene located on human chromosome 11q11-12

Husmann, Knut; Sers, Christine; Fietze, Ellen; Mincheva, Antoaneta; Lichter, Peter; Schäfer, Reinhold

doi:10.1038/sj.onc.1202060

Cited by 57 publications

(69 citation statements)

References 37 publications

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“…5,19 In contrast, we now found H-REV107-1 protein in six of nine NSCLC cell lines expressing H-REV107-1 mRNA. This observation is consistent with the idea that H-REV107-1 is deficient in its role as a tumor suppressor in NSCLCs.…”

mentioning

confidence: 90%

“…We have described earlier that expression of the H-REV107-1 protein might be controlled at the posttranscriptional levels. 5,19 Therefore, we examined the presence of H-REV107-1 protein in several cell lines showing a strong H-REV107-1 mRNA signal. We detected low levels of the H-REV107-1 protein in 9 of 12 cell lines analyzed, and four were considered to be negative, confirming that expression of this protein is controlled at both transcriptional and posttranscriptional levels ( Figure 2B).…”

Section: Impact Of Sirna-mediated H-rev107-1 Knockdown On Anchorage-dmentioning

confidence: 99%

“…5,19 To determine whether H-REV107-1 might play a role in the development of lung cancer, we investigated its expression using Figure 1A). Because of this variability in H-REV107-1 mRNA expression, we examined H-REV107-1 protein expression in normal bronchial epithelium and in a subset of NSCLCs using conventional immunohistochemistry and a lung tissue microarray.…”

Section: H-rev107-1 Expression In Normal Lungmentioning

confidence: 99%

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H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

Nazarenko

Kristiansen

Fonfara

et al. 2006

The American Journal of Pathology

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H-REV107-1 , a known member of the class II tumor suppressor gene family , is involved in the regulation of differentiation and survival. We analyzed H-REV107-1 in non-small cell lung carcinomas , in normal lung , and in immortalized and tumor-derived cell lines. Sixty-eight percent of lung tumors revealed positive H-REV107-1-specific staining. Furthermore , survival analysis demonstrated a significant association of cytoplasmic H-REV107-1 with decreased patient survival. This suggested that H-REV107-1 , known as a tumor suppressor , plays a different role in non-small cell lung carcinomas. Knock-down of H-REV107-1 expression in lung carcinoma cells inhibited anchorage-dependent and anchorage-independent growth whereas overexpression of H-REV107-1 induced tumor cell proliferation. Consistent with results of the survival analysis , cytoplasmic localization of the protein was essential for this growth-inducing function. Analysis of signaling pathways potentially involved in this process demonstrated that overexpression of H-REV107-1 stimulated RAS-GTPase activity , ERK1 ,2 phosphorylation, and caveolin-1 expression in the cell lines analyzed. These results indicate that H-REV107-1 is deficient in its function as a tumor suppressor in nonsmall cell lung carcinomas and is required for proliferation and anchorage-independent growth in cells expressing high levels of the protein, thus contributing to tumor progression in a subset of non-small cell lung carcinomas.

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confidence: 90%

Section: Impact Of Sirna-mediated H-rev107-1 Knockdown On Anchorage-dmentioning

confidence: 99%

Section: H-rev107-1 Expression In Normal Lungmentioning

confidence: 99%

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H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

Nazarenko

Kristiansen

Fonfara

et al. 2006

The American Journal of Pathology

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“…The H-REV107-1 gene is ubiquitously expressed in most normal tissues, however, expression is lost in human tumour cell lines and tumour samples (Husmann et al, 1998). To view the distribution of di erential H-REV107-1 expression in a larger set of primary and metastatic tumours, we hybridized a Cancer Pro®ling cDNA Array (Clontech TM ) with an H-REV107-1-speci®c probe.…”

Section: Down-regulation Of H-rev107-1 In Human Ovarian Carcinomasmentioning

confidence: 99%

“…H-REV107-1 mRNA is almost ubiquitously present in normal tissues, but not expressed in most human tumour cell lines (Husmann et al, 1998). Forced expression of the rat H-rev107-1 gene resulted in growth inhibition of RAS-transformed cells in vitro and in vivo (Sers et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

The class II tumour suppressor gene H-REV107-1 is a target of interferon-regulatory factor-1 and is involved in IFNγ-induced cell death in human ovarian carcinoma cells

et al. 2002

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Suppression of the TIG3 tumor suppressor gene in human ovarian carcinomas is mediated via mitogen‐activated kinase‐dependent and ‐independent mechanisms

Lotz

Kellner

Heitmann

et al. 2005

Intl Journal of Cancer

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The TIG3 gene is a retinoic acid inducible class II tumor suppressor gene downregulated in several human tumors and malignant cell lines. Diminished TIG3 expression correlates with decreased differentiation whereas forced expression of TIG3 suppresses oncogenic signaling pathways and subsequently induces differentiation or apoptosis in tumor cells. Analysis of TIG3 mRNA expression in a large set of cDNA pools derived from matched tumor and normal human tissues showed a significant downregulation of TIG3 in 29% of the cDNA samples obtained from ovarian carcinomas. Using in situ hybridization, we demonstrated expression of TIG3 in the epithelial lining of 7 normal ovaries but loss of TIG3 expression in 15/19 of human ovarian carcinoma tissues. In SKOV-3, CAOV-3 and ES-2 ovarian carcinoma cell lines, downregulation of TIG3 mRNA was reversible and dependent on an activated MEK-ERK signaling pathway. Re-expression of TIG3 mRNA in these cells upon specific interference with the MEKpathway was correlated with growth inhibition of the cells. In OVCAR-3 and A27/80 ovarian carcinoma cells, TIG3 suppression is MEK-ERK independent, but expression could be reconstituted upon interferon gamma (IFNc) induction. Overexpression of TIG3 in A27/80 ovarian carcinoma cells significantly impaired cell growth and despite increased mRNA levels, TIG3 protein was hardly detectable. These results suggest that TIG3 is negatively regulated by an activated MEK-ERK signaling pathway. Further mechanisms must interfere with TIG3 expression that are independent of MEK and partially include interferon-responsive components. ' 2005 Wiley-Liss, Inc.

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Transcriptional and translational downregulation of H-REV107, a class II tumour suppressor gene located on human chromosome 11q11-12

Cited by 57 publications

References 37 publications

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

The class II tumour suppressor gene H-REV107-1 is a target of interferon-regulatory factor-1 and is involved in IFNγ-induced cell death in human ovarian carcinoma cells

Suppression of the TIG3 tumor suppressor gene in human ovarian carcinomas is mediated via mitogen‐activated kinase‐dependent and ‐independent mechanisms

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