Molecular expression of Ly6k, a putative glycosylphosphatidyl-inositol-anchored membrane protein on the mouse testicular germ cells

Maruyama, Mayuko; Yoshitake, Hiroshi; Tsukamoto, Hiroki; Takamori, Kenji; Araki, Yoshihiko

doi:10.1016/j.bbrc.2010.09.117

Cited by 16 publications

(17 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Examples included (Figure 1F): cyclin-dependent kinase interacting protein, CKS2 , which enables proliferation under conditions of replicative stress common to malignant cells (Liberal et al, 2011); LY6K which encodes a glycosylphosphatidyl-inositol (GPI)-anchored membrane protein implicated as a biomarker in lung and esophageal carcinomas (Ishikawa et al, 2007; Maruyama et al, 2010); and RBM23 , which encodes an RNA-binding protein implicated in the regulation of estrogen-mediated transcription (Dowhan et al, 2005). Using the Molecular Signatures Database (MSigDB) (Subramanian et al, 2005) the genes bound by HSF1 in the BPLER cells, but not in either of the parental lines after heat shock, were most highly enriched in protein translation, RNA binding, metabolism, cell adhesion (Figure S1D; Table S2) and other processes vital in supporting the malignant state.…”

Section: Resultsmentioning

confidence: 99%

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

Mendillo

Santagata

Koeva

et al. 2012

Cell

620

868

View full text Add to dashboard Cite

SUMMARY Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alongside their non-transformed counterparts, we identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock. Cancer-specific genes in this program support oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation. HSP genes are integral to this program, however, many are uniquely regulated in malignancy. This HSF1 cancer program is active in breast, colon and lung tumors isolated directly from human patients and is strongly associated with metastasis and death. Thus, HSF1 rewires the transcriptome in tumorigenesis, with prognostic and therapeutic implications.

show abstract

Section: Resultsmentioning

confidence: 99%

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

Mendillo

Santagata

Koeva

et al. 2012

Cell

620

868

View full text Add to dashboard Cite

show abstract

“…The mystery of how LY6K could be both GPI-anchored and secreted was resolved in a recent study of the orthologous mouse Ly6k in which it is shown that there are two protein isoforms, one anchored and one secreted (Maruyama et al, 2010). The two Ly6k isoforms differ by a post-translational modification that changes the molecular weight, and hence they cannot be distinguished by RT-PCR or any other technique that considers the cDNA/mRNA (Maruyama et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…The two Ly6k isoforms differ by a post-translational modification that changes the molecular weight, and hence they cannot be distinguished by RT-PCR or any other technique that considers the cDNA/mRNA (Maruyama et al, 2010). …”

Section: Discussionmentioning

confidence: 99%

Genome‐wide expression and copy number analysis identifies driver genes in gingivobuccal cancers

Ambatipudi

Gerstung

Pandey

et al. 2011

Genes Chromosomes & Cancer

View full text Add to dashboard Cite

The molecular mechanisms contributing to the development and progression of gingivobuccal complex (GBC) cancers–a sub-site of oral cancer, comprising the buccal mucosa, the gingivobuccal sulcus, the lower gingival region and the retromolar trigone-remain poorly understood. Identifying the GBC cancer-related gene expression signature and the driver genes residing on the altered chromosomal regions is critical for understanding the molecular basis of its pathogenesis. Genome-wide expression profiling of 27 GBC cancers with known chromosomal alterations was performed to reveal differentially expressed genes. Putative driver genes were identified by integrating copy number and gene expression data. A total of 315 genes were found differentially expressed (P≤0.05, logFC>2.0) of which eleven genes were validated by real-time quantitative reverse transcriptase-PCR (qRT-PCR) in tumors (n=57) and normal GBC tissues (n=18). Overexpression of LY6K, in chromosome band 8q24.3, was validated by immunohistochemical (IHC) analysis. We found that 78.5% (2,417/3,079) of the genes located in regions of recurrent chromosomal alterations show copy number dependent expression indicating that copy number alteration has a direct effect on global gene expression. The integrative analysis revealed BIRC3 in 11q22.2 as a candidate driver gene associated with poor clinical outcome. Our study identified previously unreported differentially expressed genes in a homogeneous subtype of oral cancer and the candidate driver genes that may contribute to the development and progression of the disease.

show abstract

“…Однако в нашем исследовании зависимости между экспрессией РТГ и стадией болезни не обнаружено. Была определена зависимость экспрессии РТГ и того, к какой группе относится больной (первичный -42/77, плановый -22/77, прогрессирующий/рецидивирующий -7/77 (1,37-7,38) 0,1133 MAGE A3+ 2,53 (2,23-3,55) 108,5 (50-232) 4,39 (2,12-10,5) MAGE A6 -2,35 (1,9) 0,1608 73,5 (2,0) 0,0304 3,38 (1,38) 0,1789 MAGE A6+ 2,53 (2,54) 116 (50-284) 8,97 (2,50) MAGE A12 -2,31 (1,51) 0,0235 71,0 (12,0) 0,0461 2,50 (1,75) 0,0261 MAGE A12+ 2,48 (1,80-3,55) 89,5 (2,39-199,0) 4,39 (1,60-15,71) SSX1 -2,36 (2,05-2,63) 0,3438 71,0 (2,3-134,0) 0,0192 3,20 (1,37-7,38) 0,2339 SSX1+ 2,49 (2,09-3,55) 88,5 (49,0-232,0) 3,58 (1,86-20,27) Таблица 2. Число больных с экспрессией раково-тестикулярных генов (n = 77), n (%) рецидиве заболевания наблюдается повышенный уро-вень экспрессии генов PRAME, MAGE А3, MAGE A12, SSX1 и PASD1.…”

Section: Discussionunclassified

“…Кроме того, некоторые из них считаются маркерами таких злока-чественных новообразований, как рак яичников, шей-ки матки, молочной железы, легкого, мочевого пузы-ря, пищевода, меланомы, различных гематологических заболеваний и др. [9][10][11][12][13][14][15][16][17]. На сегодняшний день опи-сано более 150 семейств РТГ, которые включают око-ло 276 генов (http://www.cta.lncc.br).…”

Section: Introductionunclassified

Expression of Cancer-Testis Genes Prame, Ny-Eso1, Gage1, Mage A3, Mage A6, Mage A12, Ssx1, Sllp1, Pasd1 in Patients With Multiple Myeloma, Their Influence on Overall Survival and Relapse Rate

Солодовник¹,

Mkrtchyan²,

Misyurin³

et al. 2018

Usp. mol. onkol

View full text Add to dashboard Cite

Objective:to study the prognostic significance of the expression of cancer-testis (CT) genes PRAME, NY-ESO1, GAGE1, MAGE A3, MAGE A6, MAGE A12, SSX1, SLLP1, PASD1 in patients with multiple myeloma (MM) and their influence on overall survival and relapse rate. To determine their effect on suсh clinical parameters as levels of lactate dehydrogenase, leucocytes, hemoglobin, calcium, albumen, creatinine, beta-2-microglobulin.Materials and methods.Real-time polymerase chain reaction was performed on complementary DNA obtained from bone marrow of 77 patients with MM. The statistical analysis was performed using the Statistica 10.0 software package. To estimate prognostic values of the CT gene expression data were analyzed by the Kaplan – Meier method.Results.The study was conducted to determine the level of expression of CT genes PRAME, NY-ESO1, GAGE1, MAGE A3, MAGE A6, MAGE A12, SSX1, SLLP1, PASD1 in a group of patients with MM. The group included primary and receiving cancer treatment in MM patients. According to the log-rank criterion expression of any of the CT genes PRAME, NY-ESO1, GAGE1, MAGE A3, MAGE A6, MAGE A12, SSX1, SLLP1, PASD1 exerts a significant influence on overall survival and progression-free survival/relapse. It was also determined that providing expression of some CT genes, the levels of creatinine, calcium, beta-2-microglobulin were much higher to compare with patients without expression.

show abstract

Molecular expression of Ly6k, a putative glycosylphosphatidyl-inositol-anchored membrane protein on the mouse testicular germ cells

Cited by 16 publications

References 23 publications

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

Genome‐wide expression and copy number analysis identifies driver genes in gingivobuccal cancers

Expression of Cancer-Testis Genes Prame, Ny-Eso1, Gage1, Mage A3, Mage A6, Mage A12, Ssx1, Sllp1, Pasd1 in Patients With Multiple Myeloma, Their Influence on Overall Survival and Relapse Rate

Contact Info

Product

Resources

About