RARRES1 expression is significantly related to tumour differentiation and staging in colorectal adenocarcinoma

Wu, Chang‐Chieh; Shyu, Rong-Yaun; Chou, Jung-Mao; Jao, Shu-Wen; Chao, Pei-Chieh; Kang, Jung-Cheng; Wu, Sheng‐Tang; Huang, Shengping; Jiang, Shun-Yuan

doi:10.1016/j.ejca.2005.11.015

Cited by 45 publications

(44 citation statements)

References 26 publications

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“…We thus identified these genes as downstream transcriptional targets of RAR signaling in CRC cells (Table S1). It has previously been shown that two genes (i.e., CA2 and RARRES1) are expressed strongly in terminally differentiated cells of normal mucosal tissues and adenoma tissues but are absent from poorly differentiated CRC cells (24,25). These observations are in good agreement with our results that RAR signaling is activated during the differentiation of CRC cells (Fig.…”

Section: Resultssupporting

confidence: 83%

“…As transcriptional activation of RAR often leads to the inhibition of cell proliferation, loss of normal RAR function in the presence of physiological levels of RA is implicated in many types of cancers (3,4,8,25). On the other hand, the activation of the ERK pathway has been shown to be required for cell proliferation, and the constitutive activation of this pathway by the mutational activation of K-RAS and B-RAF is associated with a diverse range of cancers (11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 99%

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Antagonistic Interactions between Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase and Retinoic Acid Receptor Signaling in Colorectal Cancer Cells

Imajo

Kondoh

Yamamoto

et al. 2017

Molecular and Cellular Biology

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Deregulated activation of RAS/extracellular signal-regulated kinase (ERK) signaling and defects in retinoic acid receptor (RAR) signaling are both implicated in many types of cancers. However, interrelationships between these alterations in regulating cancer cell fates have not been fully elucidated. Here, we show that RAS/ERK and RAR signaling pathways antagonistically interact with each other to regulate colorectal cancer (CRC) cell fates. We show that RAR signaling activation promotes spontaneous differentiation of CRC cells, while ERK activation suppresses it. Our microarray analyses identify genes whose expression levels are upregulated by RAR signaling. Notably, one of these genes, MKP4, encoding a member of dual-specificity phosphatases for mitogen-activated protein (MAP) kinases, mediates ERK inactivation upon RAR activation, thereby promoting the differentiation of CRC cells. Moreover, our results also show that RA induction of RAR target genes is suppressed by the ERK pathway activation. This suppression results from the inhibition of RAR transcriptional activity, which is shown to be mediated through an RIP140/histone deacetylase (HDAC)-mediated mechanism. These results identify antagonistic interactions between RAS/ERK and RAR signaling in the cell fate decision of CRC cells and define their underlying molecular mechanisms.KEYWORDS ERK MAP kinase, colorectal cancer, retinoic acid receptor R etinoic acid (RA), an active derivative of vitamin A, plays an important role in the development and homeostasis of many vertebrate tissues through its regulatory effects on cell proliferation, differentiation, and apoptosis. Most of these effects are mediated by nuclear retinoid receptors, RA receptors (RARs), and retinoid X receptors (RXRs) (1, 2). The basic mechanism of RAR/RXR-mediated transcriptional regulation relies on the ability of RAR/RXR to recruit transcriptional corepressors and coactivators and involves a series of steps, as follows (2-4). (i) In the absence of ligand, RAR associates with the corepressor complex that mediates transrepression by the recruitment of histone deacetylase (HDAC). (ii) Ligand binding to RAR causes the dissociation of the corepressor complex and the recruitment of the coactivator complexes, which contain histone acetyltransferase, methyltransferase, and kinase and/or ATP-dependent chromatin remodeling activities that decompact repressive chromatin. (iii) Then, the coactivators dissociate, and the mediator complex assembles to recruit RNA polymerase II and the general transcription factors to the promoter, resulting in transcriptional initiation.Transactivation of RAR target genes often induces cell proliferation arrest, cell

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Section: Resultssupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Antagonistic Interactions between Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase and Retinoic Acid Receptor Signaling in Colorectal Cancer Cells

Imajo

Kondoh

Yamamoto

et al. 2017

Molecular and Cellular Biology

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“…pathogenesis of colorectal adenocarcinoma, as it has been reported that the downregulation of RARRES1 is associated with disease progression (33). Another study reported that tumour growth in the colon was increased in SPARC-null mice, suggesting that SPARC may possess anti-tumour properties (34).…”

Section: Discussionmentioning

confidence: 75%

Dietary vitamin B6 modulates the gene expression of myokines, Nrf2-related factors, myogenin and HSP60 in the skeletal muscle of rats

Suidasari

Uragami

Yanaka

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have suggested that vitamin B6 is an ergogenic factor. However, the role of dietary vitamin B6 in skeletal muscle has not been widely researched. The aim of the present study was to investigate the effects of dietary vitamin B6 on the gene expression of 19 myokines, 14 nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated factors, 8 myogenesis-related factors and 4 heat shock proteins (HSPs), which may serve important roles in skeletal muscles. Rats were fed a diet containing 1 (marginal vitamin B6 deficiency), 7 (recommended dietary level) or 35 mg/kg of pyridoxine (PN) HCl/ for 6 weeks. Gene expressions were subsequently analysed using reverse transcription-quantitative polymerase chain reaction. Food intake and growth were unaffected by this dietary treatment. The rats in the 7 and 35 mg/kg PN HCl groups exhibited a significant increase in the concentration of pyridoxal 5'-phosphate in the gastrocnemius muscle compared with the 1 mg/kg PN HCl diet (P<0.01). The expressions of myokines, such as IL-7, IL-8, secreted protein acidic and rich in cysteine, IL-6, growth differentiation factor 11, myonectin, leukaemia inhibitory factor, apelin and retinoic acid receptor responder (tazarotene induced) 1, the expression of Nrf2 and its regulated factors, such as heme oxygenase 1, superoxide dismutase 2, glutathione peroxidase 1 and glutathione S-transferase, and the expression of myogenin and HSP60 were significantly elevated in the 7 mg/kg PN HCl group compared with the 1 mg/kg PN HCl diet (P<0.05). No significant differences in levels of these genes were observed between the 35 and 1 mg/kg PN HCl, with the exception of GDF11 and myonectin, whose expressions were significantly increased in the 35 mg/kg PN HCl (P<0.05). Notably, the majority of gene expressions that were affected responded to dietary supplemental vitamin B6 in a similar manner. The results suggest that compared with the marginal vitamin B6 deficiency, the recommended dietary intake of vitamin B6 upregulates the gene expression of a number of factors that promote the growth and repair of skeletal muscle. IntroductionPyridoxal 5'-phosphate (PLP), the active form of vitamin B6, is known to modulate important metabolisms in the body (1). Skeletal muscle is the major source of PLP in the body (1). Some biological functions of vitamin B6 have been reported to be associated with fuel metabolism during exercise (2). It has been suggested that the exercise-related function of vitamin B6 is at least in part associated with the breakdown of muscle glycogen (2). Glycogen phosphorylase is the enzyme responsible for the release of glucose-1-phosphate from muscle glycogen, and PLP is a cofactor for this enzyme (2). Vitamin B6 deficiency has been reported to decrease the activity and amount of muscle phosphorylase (3). Rats fed high levels of vitamin B6 have previously exhibited elevated concentrations of muscle phosphorylase (4

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“…RARRES1, overexpressed in G3 samples, is downregulated in colorectal cancer progressive disease [22] . How- CDCP1 CAB025637 ENSG00000163814 CDCP1 HPA010978 ENSG00000163814 CDCP1 HPA010979 ENSG00000163814 CP CAB008591 ENSG00000047457 CP HPA001834 ENSG00000047457 GJB6 HPA014846 ENSG00000121742 IL1R2 HPA027597 ENSG00000115590 IL1R2 HPA027598 ENSG00000115590 IL20RB HPA019772 ENSG00000174564 IL20RB HPA019772 ENSG00000174564 ITGAV CAB002499 ENSG00000138448 ITGAV HPA004856 ENSG00000138448 LAMB3 HPA008069 ENSG00000196878 MFI2 HPA004880 ENSG00000163975 PSAT1 CAB014882 ENSG00000135069 PSAT1 CAB040567 ENSG00000135069 PTHLH CAB000072 ENSG00000087494 RARRES1 HPA003892 ENSG00000118849 SERPINA3 CAB016647 ENSG00000196136 SERPINA3 HPA002560 ENSG00000196136 SLC12A8 HPA031123 ENSG00000221955 SLPI CAB002303 ENSG00000124107 SLPI HPA027774 ENSG00000124107 SPOCK1 HPA007450 ENSG00000152377 UCHL1 CAB002580 ENSG00000154277 UCHL1 HPA005993 ENSG00000154277 Symbol Antibody ID Probe ID AQP9 -205568_at FLJ20920 -218844_at GFPT2_1 -205100_at SAA1 -214456_x_at SAA1_SAA2 -208607_s_at O f five genes the Protein Atlas database has not yet provided IHC images.…”

Section: Discussionmentioning

confidence: 99%

Putative Biomarker Genes for Grading Clear Cell Renal Cell Carcinoma

Maruschke

Koczan²,

Reuter³

et al. 2011

Urol Int

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Objective: The initial objective of this renal cancer study was to identify gene sets in clear cell renal cell carcinoma (ccRCC) to support grading of ccRCC histopathology. Materials and Methods: Preselected ccRCC tumor tissues of grade 1 (G1, n = 14) and grade 3 (G3, n = 15) as well es 14 normal kidney tissues thereof were subjected to microarray expression analysis using Human Genome U133 Plus 2.0 Array. Event ratio scoring, hierarchical clustering and principal component analysis were used to determine gene sets that distinguish expression profiles from normal kidney tissue, G1 and G3 tumor tissues. Results: An initial set of 73 genes provided seven gene subclusters (SC01 to SC07) that distinguish RNA expression profiles from G1, G3 tumor and normal kidney tissues. A ranked list of 24 genes was determined that separated G1 from G3 tumors in high concordance with histopathological grading confirmed by immunohistochemical analysis of ceruloplasmin protein expression. Conclusion: A final set of 24 genes has been determined awaiting further validation on the RNA as well as on the protein level by studying an additional cohort of ccRCC patients. A reliable separation of G1 and G3 tumor grades will be instrumental to foster and direct the administration of upcoming targeted therapeutics of ccRCC tumors in a more predictive and reliable manner.

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RARRES1 expression is significantly related to tumour differentiation and staging in colorectal adenocarcinoma

Cited by 45 publications

References 26 publications

Antagonistic Interactions between Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase and Retinoic Acid Receptor Signaling in Colorectal Cancer Cells

Antagonistic Interactions between Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase and Retinoic Acid Receptor Signaling in Colorectal Cancer Cells

Dietary vitamin B6 modulates the gene expression of myokines, Nrf2-related factors, myogenin and HSP60 in the skeletal muscle of rats

Putative Biomarker Genes for Grading Clear Cell Renal Cell Carcinoma

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