cDNA Microarray Analysis of Vestibular Schwannomas

Welling, D. Bradley; Lasak, John M.; Akhmametyeva, Elena M.; Ghaheri, Bobak A.; Chang, Long-Sheng

doi:10.1097/00129492-200209000-00022

Cited by 99 publications

(88 citation statements)

References 58 publications

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“…Previous studies suggest that frequently reduced RBM5 levels exist in different types of tumors including breast cancer (25), schwannoma (26), and ~75% of primary lung cancers (27). We previously reported that the protein levels of RBM5 are lower in NSCLC compared with non-tumorous tissues (13).…”

Section: Discussionmentioning

confidence: 86%

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

Hao

et al. 2015

Oncology Reports

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Abstract. Cigarette smoking is closely associated with various respiratory diseases. Oxidants and carcinogens in cigarettes are reported to induce various airway epithelial injuries. However, the underlying mechanisms remain unclear. The aims of the present study were to determine the involvement of RNA-binding motif protein 5 (RBM5) and Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury, as well as the interaction between both. A549 cells were treated with cigarette smoke extract (CSE). The MTT assay was used to assess the effects of CSE on cell viability. The levels of RBM5 and Wnt/β-catenin/GSK3β were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis. A luciferase assay was used to assess the activity of β-catenin/T-cell factor (TCF) signaling. The results revealed that CSE inhibited A549 cell viability in both a dose-and time-dependent manner. Cytosolic and nuclear β-catenin levels were significantly increased following CSE treatment, compared with those in the control cells (P<0.05). The luciferase activity in CSE-exposed cells transfected with the TCF luciferase reporter wild-type plasmid (pGL3-OT) was significantly greater than that in cells without CSE exposure (33,167±3,085 vs. 19,978±1,916, respectively, P<0.05). Both the mRNA and protein levels of RBM5 in the CSE-treated cells were significantly reduced compared to the levels in the controls (all P<0.05). The overexpression of RBM5 inhibited Wnt/β-catenin signaling in the A549 cells, while silencing of RBM5 enhanced Wnt/β-catenin signaling. The β-catenin/TCF signaling inhibitor ICG-001 had no apparent effect on the RBM5 levels. Downregulation of RBM5 and activation of Wnt/β-catenin signaling are involved in CSE-induced alveolar epithelial injury. RBM5 acts as an upstream molecule that negatively regulates the activity of Wnt/β-catenin signaling.

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Section: Discussionmentioning

confidence: 86%

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

Hao

et al. 2015

Oncology Reports

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“…Briefly, 5 μg of total RNA was primed with 500 ng of oligo(dT) [12][13][14][15][16][17][18] in a total of 12 μl reaction volume for 10 min. at 70°C followed by quick chill on ice.…”

Section: Rt-pcrmentioning

confidence: 99%

“…For example, H37 was identified as a serum antigen reacting with autologous antibody in renal cancer [13]. H37 is downregulated in human schwannomas [14] and in rastransformed Rat-1 embryonic fibroblasts [15]. Ectopic expression of H37 also suppresses growth of HT 1080 fibrosarcoma cells [15].…”

Section: Introductionmentioning

confidence: 99%

The two single nucleotide polymorphisms in the H37/RBM5 tumour suppressor gene at 3p21.3 correlated with different subtypes of non-small cell lung cancers

Koegel

Phan

et al. 2007

Lung Cancer

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SummaryAllele loss and genetic alteration in chromosome 3p, particularly in 3p21.3 region, are the most frequent and the earliest genomic abnormalities found in lung cancer. Multiple 3p21.3 genes exhibit various degrees of tumour suppression activity suggesting that 3p21.3 genes may function as an integrated tumour suppressor region through their diverse biological activities. We have previously demonstrated growth inhibitory effects and tumour suppression mechanism of the H37/RBM5 gene which is one of the 19 genes residing in the 370kb minimal overlap region at 3p21.3. In the current study, in an attempt to find, if any, mutations in the H37 coding region in lung cancer cells, we compared nucleotide sequences of the entire H37 gene in tumour vs. adjacent normal tissues from 17 non-small cell lung cancer (NSCLC) patients. No mutations were detected, instead, we found the two silent single nucleotide polymorphisms (SNPs), C1138T and C2185T, within the coding region of the H37 gene. In addition, we found that specific allele types at these SNP positions are correlated with different histological subtypes of NSCLC; tumours containing heterozygous alleles (C+T) at these SNP positions are more likely to be associated with adenocarcinoma (AC) whereas homozygous alleles (either C or T) are associated with squamous cell carcinoma (SCC) (p=0.0098). We postulate that, these two silent polymorphisms may be in linkage disequilibrium (LD) with a disease causative allele in the 3p21.3 tumour suppressor region which is packed with a large number of important genes affecting lung cancer development. In addition, because of prevalent loss of heterozygosity (LOH) detected at 3p21.3 which precedes lung cancer initiation, these SNPs may be developed into a marker screening for the high risk individuals. Keywords lung cancer; H37/RBM5/Luca15; single nucleotide polymorphism; 3p21.3; tumour suppressor gene; linkage disequilibrium; loss of heterozygosity

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“…The RNA-binding motif protein 5 gene ( RBM5/LUCA-15/H37 ) encodes a protein containing two RRMs, two zinc fingers, one arginine-serine-rich domain (RS) and one glycine patch (G-patch) [15]. RBM5 and its paralog RBM6 are located in the human chromosome 3p21.3 region and were identified as candidate tumor suppressors of lung cancers and other solid tumors [16–22]. RBM10 , another paralog of RBM5 , is also frequently mutated in lung adenocarcinoma samples [23].…”

Section: Introductionmentioning

confidence: 99%

RBM-5 modulates U2AF large subunit-dependent alternative splicing inC. elegans

Zhou

Gao

et al. 2018

RNA Biology

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A key step in pre-mRNA splicing is the recognition of 3ʹ splicing sites by the U2AF large and small subunits, a process regulated by numerous trans-acting splicing factors. How these trans-acting factors interact with U2AF in vivo is unclear. From a screen for suppressors of the temperature-sensitive (ts) lethality of the C. elegans U2AF large subunit gene uaf-1(n4588) mutants, we identified mutations in the RNA binding motif gene rbm-5, a homolog of the tumor suppressor gene RBM5. rbm-5 mutations can suppress uaf-1(n4588) ts-lethality by loss of function and neuronal expression of rbm-5 was sufficient to rescue the suppression. Transcriptome analyses indicate that uaf-1(n4588) affected the expression of numerous genes and rbm-5 mutations can partially reverse the abnormal gene expression to levels similar to that of wild type. Though rbm-5 mutations did not obviously affect alternative splicing per se, they can suppress or enhance, in a gene-specific manner, the altered splicing of genes in uaf-1(n4588) mutants. Specifically, the recognition of a weak 3ʹ splice site was more susceptible to the effect of rbm-5. Our findings provide novel in vivo evidence that RBM-5 can modulate UAF-1-dependent RNA splicing and suggest that RBM5 might interact with U2AF large subunit to affect tumor formation.

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cDNA Microarray Analysis of Vestibular Schwannomas

Cited by 99 publications

References 58 publications

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

The two single nucleotide polymorphisms in the H37/RBM5 tumour suppressor gene at 3p21.3 correlated with different subtypes of non-small cell lung cancers

RBM-5 modulates U2AF large subunit-dependent alternative splicing inC. elegans

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