Decreased Hrad6B expression in lung cancer

Sasaki, Hidefumi; Moriyama, Satoru; Nakashima, Yoshiaki; Yukiue, Haruhiro; Fukai, Ichiro; Fujii, Yoshitaka

doi:10.1080/02841860410014920

Cited by 11 publications

(7 citation statements)

References 20 publications

(15 reference statements)

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“…UBE2B is also called HHR6B or RAD6B, and is the human homologue of yeast Rad6B . Although the expression and function of UBE2B have been reported in various human cancers , the role of UBE2B in OSCC remains unclear. We analysed ten clinical samples and all revealed that UBE2B expression is lower in the tumour tissues than in the normal tissues.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of miR‐455‐5p by the TGF‐β–SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B

Cheng

Shiah

Huang

et al. 2016

The Journal of Pathology

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MicroRNAs (miRNAs) are involved in the tumourigenesis of various cancers by regulating their downstream targets. To identify the changes of miRNAs in oral squamous cell carcinoma (OSCC), we investigated the expression profiles of miRNAs in 40 pairs of OSCC specimens and their matched non-tumour epithelial tissues. Our data revealed higher miR-455-5p expression in the tumour tissues than in the normal tissues; the expression was also higher in oral cancer cell lines than in normal keratinocyte cell lines. MiR-455-5p knockdown reduced both the anchorage-independent growth and the proliferative ability of oral cancer cells, and these factors increased in miR-455-5p-overexpressing cells. Furthermore, by analysing the array data of patients with cancer and cell lines, we identified ubiquitin-conjugating enzyme E2B (UBE2B) as a target of miR-455-5p, and further validated this using 3'-untranslated region luciferase reporter assays and western blot analysis. We also demonstrated that UBE2B suppression rescued the impaired growth ability of miR-455-5p-knockdown cells. Furthermore, we observed that miR-455-5p expression was regulated, at least in part, by the transforming growth factor-β (TGF-β) pathway through the binding of SMAD3 to specific promoter regions. Notably, miR-455-5p expression was associated with the nodal status, stage, and overall survival in our patients, suggesting that miR-455-5p is a potential marker for predicting the prognosis of patients with oral cancer. In conclusion, we reveal that miR-455-5p expression is regulated by the TGF-β-dependent pathway, which subsequently leads to UBE2B down-regulation and contributes to oral cancer tumourigenesis. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 99%

Up‐regulation of miR‐455‐5p by the TGF‐β–SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B

Cheng

Shiah

Huang

et al. 2016

The Journal of Pathology

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“…Human homologues of yeast Rad 6 (Hrad6B) encode ubiq-uitin-conjugating enzymes, and is highly expressed in lung cancer cell. It has been reported that DNA repair and UV mutagenesis are defective in Saccharomyces cerevisiae rad6 mutant (13). Peroxiredoxin-1 is the most ubiquitously expressed member of the peroxiredoxin family, and is found in the cytoplasm, nucleus, mitochondria, and peroxisomes of many cell types (14).…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profile during Chondrogenesis in Human Bone Marrow derived Mesenchymal Stem Cells using a cDNA Microarray

et al. 2011

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Mesenchymal stem cells (MSCs) have the capacity to proliferate and differentiate into multiple connective tissue lineages, which include cartilage, bone, and fat. Cartilage differentiation and chondrocyte maturation are required for normal skeletal development, but the intracellular pathways regulating this process remain largely unclear. This study was designed to identify novel genes that might help clarify the molecular mechanisms of chondrogenesis. Chondrogenesis was induced by culturing human bone marrow (BM) derived MSCs in micromass pellets in the presence of defined medium for 3, 7, 14 or 21 days. Several genes regulated during chondrogenesis were then identified by reverse transcriptase-polymerase chain reaction (RT-PCR). Using an ABI microarray system, we determined the differential gene expression profiles of differentiated chondrocytes and BM-MSCs. Normalization of this data resulted in the identification of 1,486 differentially expressed genes. To verify gene expression profiles determined by microarray analysis, the expression levels of 10 genes with high fold changes were confirmed by RT-PCR. Gene expression patterns of 9 genes (Hrad6B, annexinA2, BMP-7, contactin-1, peroxiredoxin-1, heat shock transcription factor-2, synaptotagmin IV, serotonin receptor-7, Axl) in RT-PCR were similar to the microarray gene expression patterns. These findings provide novel information concerning genes involved in the chondrogenesis of human BM-MSCs.

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“…Analyses of lung cancer tissue versus normal tissue for human Rad6 expression by Sasaki et al. (2004) revealed reduced Rad6 expression in the cancerous tissues.…”

Section: Role Of Chromatin Remodeling In Human Tumorsmentioning

confidence: 99%

“…(2004) revealed reduced Rad6 expression in the cancerous tissues. It has been proposed that Rad6 plays a role in DNA damage tolerance in yeast which might also be possible for the human homologue (Table 2) (Sasaki et al., 2004). Studies of Xeroderma Pigmentosum group E cells, which are characterized by defects in nucleotide excision repair, showed a correlation between defective H2A ubiquitination and DNA repair after UV treatment (Kapetanaki et al., 2006).…”

Section: Role Of Chromatin Remodeling In Human Tumorsmentioning

confidence: 99%

Epigenetic events in malignant melanoma

Rothhammer

Bosserhoff

2007

Pigment Cell Research

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Irreversible changes in the DNA sequence, including chromosomal deletions or amplification, activating or inactivating mutations in genes, have been implicated in the development and progression of melanoma. However, increasing attention is being turned towards the participation of 'epigenetic' events in melanoma progression that do not affect DNA sequence, but which nevertheless may lead to stable inherited changes in gene expression. Epigenetic events including histone modifications and DNA methylation play a key role in normal development and are crucial to establishing the correct program of gene expression. In contrast, mistargeting of such epigenetic modifications can lead to aberrant patterns of gene expression and loss of anti-cancer checkpoints. Thus, to date at least 50 genes have been reported to be dysregulated in melanoma by aberrant DNA methylation and accumulating evidence also suggests that mistargetting of histone modifications and altered chromatin remodeling activities will play a key role in melanoma. This review gives an overview of the many different types of epigenetic modifications and their involvement in cancer and especially in melanoma development and progression.

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Decreased Hrad6B expression in lung cancer

Cited by 11 publications

References 20 publications

Up‐regulation of miR‐455‐5p by the TGF‐β–SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B

Up‐regulation of miR‐455‐5p by the TGF‐β–SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B

Gene Expression Profile during Chondrogenesis in Human Bone Marrow derived Mesenchymal Stem Cells using a cDNA Microarray

Epigenetic events in malignant melanoma

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