LUCA-15 suppresses CD95-mediated apoptosis in Jurkat T cells

Sutherland, Leslie C.; Lerman, Michael I.; Williams, Gwyn T.; Miller, Barbara A.

doi:10.1038/sj.onc.1204371

Cited by 32 publications

(28 citation statements)

References 42 publications

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“…Decreased SOCS gene expression due to promoter methylation has been observed in advanced human cancers including melanoma [1][2][3][4][5][6][7]. In agreement with a proposed role in tumor suppression, SOCS1-deficient mice show myeloproliferative disorders and lymphomas [8][9][10].…”

Section: Introductionmentioning

confidence: 60%

Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells

Parrillas

Martínez-Muñoz

Holgado

et al. 2012

Cell. Mol. Life Sci.

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Hypermethylation of SOCS genes is associated with many human cancers, suggesting a role as tumor suppressors. As adaptor molecules for ubiquitin ligases, SOCS proteins modulate turnover of numerous target proteins. Few SOCS targets identified so far have a direct role in cell cycle progression; the mechanism by which SOCS regulate the cell cycle thus remains largely unknown. Here we show that SOCS1 overexpression inhibits in vitro and in vivo expansion of human melanoma cells, and that SOCS1 associates specifically with Cdh1, triggering its degradation by the proteasome. Cells therefore show a G1/S transition defect, as well as a secondary blockade in mitosis and accumulation of cells in metaphase. SOCS1 expression correlated with a reduction in cyclin D/E levels and an increase in the tumor suppressor p19, as well as the CDK inhibitor p53, explaining the G1/S transition defect. As a result of Cdh1 degradation, SOCS1-expressing cells accumulated cyclin B1 and securin, as well as apparently inactive Cdc20, in mitosis. Levels of the late mitotic Cdh1 substrate Aurora A did not change. These observations comprise a hitherto unreported mechanism of SOCS1 tumor suppression, suggesting this molecule as a candidate for the design of new therapeutic strategies for human melanoma.

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Section: Introductionmentioning

confidence: 60%

Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells

Parrillas

Martínez-Muñoz

Holgado

et al. 2012

Cell. Mol. Life Sci.

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“…RBM5 can increase the expression of proapoptotic protein BAX and reduce that of anti-apoptotic proteins including BCL-2 and BCL-XL [26–28]. It could also affect the expression of other apoptosis and cell cycle genes [29].…”

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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“…Ectopic expression of H37 also suppresses growth of HT 1080 fibrosarcoma cells [15]. Alternatively-spliced transcripts from the H37 locus and antisense fragments also serve as apoptotic regulators in hematopoetic cells [16][17][18][19][20]. Most significantly, the H37/RBM5 gene was included in the 17 common gene signature associated with metastasis (one of the nine genes down-regulated in metastases) identified in multiple solid tumour types [21].…”

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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LUCA-15 suppresses CD95-mediated apoptosis in Jurkat T cells

Cited by 32 publications

References 42 publications

Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells

Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells

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

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

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