CREPT/RPRD1B, a Recently Identified Novel Protein Highly Expressed in Tumors, Enhances the β-Catenin·TCF4 Transcriptional Activity in Response to Wnt Signaling

Zhang, Yanquan; Liu, Chunxiao; Duan, Xiaolin; Ren, Fei; Li, Shan; Jin, Zhe; Wang, Yinyin; Feng, Yarui; Liu, Zewen; Chen, Zhijie

doi:10.1074/jbc.m114.560979

Cited by 43 publications

(68 citation statements)

References 34 publications

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“…These results suggest that mammalian p15RS functions differently from its yeast homolog Rtt103. Intriguingly, the role of p15RS in the regulation of gene transcription also differs from that of CREPT as we observed that CREPT binds to both the promoter and termination region of the CCND1 gene (24) and promotes Wnt signaling (40). However, the differential roles of p15RS and CREPT in regulating gene transcription were not elucidated by partial structural analyses (23,25,27).…”

Section: Discussionmentioning

confidence: 50%

“…Although yeast Rtt103 was demonstrated to be a gene that favors cell growth (as the double deletion of Rtt103 is synthetic lethal) (39) and human/mouse CREPT promotes tumor cell proliferation (24,40), p15RS was reported to inhibit cell growth as demonstrated by both Liu et al (22) and Chang and co-workers (29). Interestingly, although yeast Rtt103 binds only to the 3Ј-end of genes to regulate transcriptional termination by a mechanism called the Torpedo model, our results indicated that p15RS preferably binds to the promoter regions of the c-MYC and CCDN1 genes as shown here (Fig.…”

Section: Discussionmentioning

confidence: 99%

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p15RS/RPRD1A (p15INK4b-related Sequence/Regulation of Nuclear Pre-mRNA Domain-containing Protein 1A) Interacts with HDAC2 in Inhibition of the Wnt/β-Catenin Signaling Pathway

Liu

Zhang

et al. 2015

Journal of Biological Chemistry

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Background: p15RS/RPRD1A inhibits Wnt/␤-catenin signaling by recruiting HDAC2. Results: p15RS interacts with HDAC2 and enhances the occupancy of HDAC2 to promoters of Wnt-targeted genes, keeping histone3 in a deacetylated state. Conclusion: p15RS cooperates with HADC2 in the inhibition of Wnt/␤-catenin signaling. Significance: p15RS/HDAC2 is a novel co-repressor in the regulation of Wnt/␤-catenin signaling.

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Section: Discussionmentioning

confidence: 50%

Section: Discussionmentioning

confidence: 99%

p15RS/RPRD1A (p15INK4b-related Sequence/Regulation of Nuclear Pre-mRNA Domain-containing Protein 1A) Interacts with HDAC2 in Inhibition of the Wnt/β-Catenin Signaling Pathway

Liu

Zhang

et al. 2015

Journal of Biological Chemistry

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“…However, the suggestive association of RPRD1B with docetaxel-induced neuropathy, indicates that other mechanisms may be important. RPRD1B functions as a co-activator of the β-catenin-TCF complex to enhance the transcriptional activity of Wnt signaling (48). Wnt signaling is critical for initial neural cell-fate determination, patterning and synapse formation of sensory neurons of the dorsal root ganglia.…”

Section: Discussionmentioning

confidence: 99%

Clinical and Genome-Wide Analysis of Cisplatin-Induced Peripheral Neuropathy in Survivors of Adult-Onset Cancer

Dolan

Charif

Wheeler

et al. 2017

Clinical Cancer Research

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Purpose Our purpose was to characterize the clinical influences, genetic risk factors, and gene mechanisms contributing to persistent cisplatin-induced peripheral neuropathy (CisIPN) in testicular cancer survivors (TCS). Experimental Design TCS given cisplatin-based therapy completed the validated EORTC QLQ-CIPN20 questionnaire. An ordinal CisIPN phenotype was derived and associations with age, smoking, excess drinking, hypertension, body mass index, diabetes, hypercholesterolemia, cumulative cisplatin dose, and self-reported health were examined for 680 TCS. Genotyping was performed on the Illumina HumanOmniExpressExome chip. Following quality control and imputation, 5.1 million SNPs in 680 genetically European TCS formed the input set. GWAS and PrediXcan were used to identify genetic variation and genetically-determined gene expression traits, respectively, contributing to CisIPN. We evaluated two independent datasets for replication: Vanderbilt’s electronic health database, BioVU and CALGB 90401 trial. Results Eight sensory items formed a subscale with good internal consistency (Cronbach α=0.88). Variables significantly associated with CisIPN included age at diagnosis (OR per year=1.06, p=2 × 10−9), smoking (OR=1.54, p=0.004), excess drinking (OR=1.83, p=0.007), and hypertension (OR=1.61, p=0.03). CisIPN was correlated with lower self-reported health (OR=0.56; p=2.6 × 10−9) and weight gain adjusted for years since treatment (OR per Δkg/m2=1.05, p=0.004). PrediXcan identified lower expressions of MIDN and RPRD1B, and higher THEM5 expression as associated with CisIPN (p-value for each < 5 × 10−6) with replication of RPRD1B meeting significance criteria (Fisher’s combined p=0.0089). Conclusions CisIPN is associated with age, modifiable risk factors and genetically-determined expression level of RPRD1B. Further study of implicated genes could elucidate the pathophysiologic underpinnings of CisIPN.

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“…The human gastric adenocarcinoma cell line (MGC803) expressing CREPT stably was applied as positive control [6], and the normal human oral keratinocyte cell line (HOK) as normal control[10, 20, 21]. SCC25, CAL27 and HOK were obtained from the American type culture collection (ATCC).…”

Section: Methodsmentioning

confidence: 99%

“…Similar to cyclin D1, the expression of a series of cell cycle-related factors, such as cyclin E, CDK2, CDK4 and CKD6, are also promoted by CREPT in the same manner [9]. Additionally, recent studies also revealed that CREPT could stabilize the binding of β-catenin/TCF4 complex to the promoters of cyclin D1 and c-Myc, which enforced the effects of Wnt canonical signaling on cell cycle [10]. Besides the enhancement on tumorigenesis, CREPT also plays a critical role in the activation of peripheral T cells, keratinocyte differentiation and metastasis by regulating cell cycle-related genes [11].…”

Section: Introductionmentioning

confidence: 99%

Knocking-down of CREPT prohibits the progression of oral squamous cell carcinoma and suppresses cyclin D1 and c-Myc expression

Ren

Zhang

et al. 2017

PLoS ONE

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BackgroundAs a regulator essential for many cell cycle-related proteins, the robust expression of Cell cycle-Related and Expression-elevated Protein in Tumor (CREPT) implicates a poor diagnosis of endoderm and mesoderm-derived tumors. Whether CREPT plays the same role in the tumorigenesis derived from ectodermal tissues remains elusive.MethodsTo explore the role of CREPT in ectoderm-derived tumors, cells from 7oral squamous cell carcinoma (OSCC) lines and 84clinical OSCC samples were exploited in this study. Quantitative PCR, Western blot assay and immunohistochemistry were applied in the evaluation of CREPT, cyclin D1 and c-Myc expression. Knocking-down of CREPT was performed by lentivirus delivering specific shRNA of CREPT. The effects of CREPT on OSCC were examined by cell proliferation, colony formation, apoptosis, cell migration and xenograft implantation experiments.ResultsCompared with human normal oral keratinocytes, OSCC cell lines showed a significantly elevated expression of CREPT in both mRNA and protein levels. Consistently, samples from OSCC patients also exhibited a noticeably stronger CREPT expression than the noncancerous samples. In contrast, knocking down of CREPT in OSCC cell lines significantly reduced proliferation, colony formation and migration as well as the expression of cyclin D1 and c-Myc, but promoted apoptosis. Statistical analysis also suggested that CREPT expression was significantly correlated with the T and N classification of OSCC. Furthermore, CAL27 mouse xenograft model confirmed that down-regulation of CREPT prohibited cyclin D1 and c-Myc expression, through which decreased the in vivo tumor growth, but increased the survival ratio of hosts.ConclusionIn OSCC cell lines, up-regulated CREPT expression enhanced cell proliferation, migration and cell cycle as well as promoted cyclin D1 and c-Myc expression as it did in endoderm and mesoderm-origin tumors. Our study strongly suggests that CREPT could be used as a marker for the OSCC prognosis and might work as a potential target in future OSCC therapy.

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CREPT/RPRD1B, a Recently Identified Novel Protein Highly Expressed in Tumors, Enhances the β-Catenin·TCF4 Transcriptional Activity in Response to Wnt Signaling

Cited by 43 publications

References 34 publications

p15RS/RPRD1A (p15INK4b-related Sequence/Regulation of Nuclear Pre-mRNA Domain-containing Protein 1A) Interacts with HDAC2 in Inhibition of the Wnt/β-Catenin Signaling Pathway

p15RS/RPRD1A (p15INK4b-related Sequence/Regulation of Nuclear Pre-mRNA Domain-containing Protein 1A) Interacts with HDAC2 in Inhibition of the Wnt/β-Catenin Signaling Pathway

Clinical and Genome-Wide Analysis of Cisplatin-Induced Peripheral Neuropathy in Survivors of Adult-Onset Cancer

Knocking-down of CREPT prohibits the progression of oral squamous cell carcinoma and suppresses cyclin D1 and c-Myc expression

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