Correlation between expression of cellular retinol-binding protein 1 and its methylation status in larynx cancer

Peralta, Raúl; Valdivia, Alejandra; Alvarado‐Cabrero, Isabel; Gallegos, Francisco; Apresa, Teresa; Hernández, D.; Mendoza, Mónica; Romero, Pablo; Paniagua, Lucero; Ibáñez, Miguel Martín-Luquero; Cabrera, Lourdes; Salcedo, Mauricio

doi:10.1136/jclinpath-2011-200304

Cited by 10 publications

(8 citation statements)

References 23 publications

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“…Since both STC2 and SLCO3A1 are thought to have oncogenic roles in cancer they were considered inappropriate for further investigation in our study. On the other hand, decreased expression of CRBP1 or hypermethylation of the CRBP1 promoter have been reported in multiple cancers in several reports (Esteller et al , 2002; Yamashita et al , 2002; Jerónimo et al , 2004; Kwong et al , 2005; Toki et al , 2010; Colvin et al , 2011; Peralta et al , 2012; Mendoza-Rodriguez et al , 2013). Analysis of the expression of CRBP1 in CRC cell lines suggested that it may have a functional role in radiation sensitivity in at least four cell lines.…”

Section: Discussionmentioning

confidence: 97%

“…Connected with this finding, there was one clinical sample of a rectal cancer case that showed grade 3 after NCRT, but in which there was high CRBP1 promoter DNA methylation. Qualitative or semi-quantitative analyses of CRBP1 promoter methylation have been reported in several studies (Jerónimo et al , 2004; Kwong et al , 2005; Toki et al , 2010; Peralta et al , 2012; Mendoza-Rodriguez et al , 2013). In this study, we performed quantitative analysis by using qMSP.…”

Section: Discussionmentioning

confidence: 98%

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Comprehensive molecular exploration identified promoter DNA methylation of the CRBP1 gene as a determinant of radiation sensitivity in rectal cancer

et al. 2017

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Background:Neoadjuvant chemoradiotherapy (NCRT) for advanced rectal cancer (RC) is a well-evidenced therapy; however, some RC patients have no therapeutic response. Patient selection for NCRT so that non-responsive patients are excluded has been subjective. To date, no molecular markers indicating radiation sensitivity have been reported.Methods:We irradiated six colorectal cancer (CRC) cell lines and identified HCT116 cells as radiation-sensitive and HCT15 and DLD-1 cells as radiation resistant. Using a microarray, we selected candidate radiation sensitivity marker genes by choosing genes whose expression was consistent with a radiation-resistant or sensitive cell phenotype.Results:Among candidate genes, cellular retinol binding protein 1 (CRBP1) was of particular interest because it was not only induced in HCT116 cells by tentative 10 Gy radiation treatments, but also its expression was increased in HCT116-derived radiation-resistant cells vs parental cells. Forced expression of CRBP1 decreased the viability of both HCT15 and DLD-1 cells in response to radiation therapy. We also confirmed that CRBP1 was epigenetically silenced by hypermethylation of its promoter DNA, and that the quantitative methylation value of CRBP1 significantly correlated with histological response in RC patients with NCRT (P=0.031).Conclusions:Our study identified CRBP1 as a radiation-sensitive predictor in RC.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Comprehensive molecular exploration identified promoter DNA methylation of the CRBP1 gene as a determinant of radiation sensitivity in rectal cancer

et al. 2017

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“…The last gene in Table 2, RBP1, encodes the carrier protein involved in the intracellular transport of retinol. Methylation-based functional loss of RBP1 has been observed in multiple cancers, and it may have potential for cancer prevention and therapy (Esteller et al, 2002;Toki et al, 2010;Peralta et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…MutL Homolog 1 Kane, et al, 1997Cunningham, et al, 1998Weisenberger, et al, 2006 BCL2/Adenovirus E1B 19kDa Interacting Protein 3 Murai, et al, 2005Shimizu, et al, 2010Liu, et al, 2011 CHFR Checkpoint with forkhead and ring finger domains, E3 ubiquitin protein ligase Morioka, et al, 2006Tanaka, et al, 2011 MGMT O-6-methylguanine-DNA methyltransferase Nakamura, et al, 2001Gerson 2004Ogino, et al, 2007Nagasaka, et al, 2008Hibi, et al, 2009Hawkins, et al, 2009 Helicase-like transcription factor Moinova, et al, 2002Herbst, et al, 2009Sandhu, et al, 2012 Retinol binding protein 1, cellular Esteller, et al, 2002Toki, et al, 2010Peralta, et al, 2012 Overexpression of both genes has been widely reported in many cancer types, including CRC (Maurer et al, 1998;Braun et al, 2001;Holbro et al, 2003;Zhou et al, 2004). The MAPK pathway is a common downstream target of the ErbB signaling pathway.…”

Section: Mlh1mentioning

confidence: 99%

Heterogeneous DNA methylation contributes to tumorigenesis through inducing the loss of coexpression connectivity in colorectal cancer

Wang

Jia

Cheng

et al. 2014

Genes Chromosomes & Cancer

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Increasing evidence indicates the high heterogeneity of cancer cells. Recent studies have revealed distinct subtypes of DNA methylation in colorectal cancer (CRC); however, the mechanism of heterogeneous methylation remains poorly understood. Gene expression is a natural, intermediate quantitative trait that bridges genotypic and phenotypic features. In this work, we studied the role of heterogeneous DNA methylation in tumorigenesis via gene expression analyses. Specifically, we integrated methylation and expression data in normal and tumor tissues, and examined the perturbations in coexpression patterns. We found that the heterogeneity of methylation leads to significant loss of coexpression connectivity in CRC; this finding was validated in an independent cohort. Functional analyses showed that the lost coexpression partners participate in important cancer-related pathways/networks, such as ErbB and mitogen-activated protein kinase (MAPK) signaling pathways. Our analyses suggest that the loss of coexpression connectivity induced by methylation heterogeneity might play an important role in CRC. To our knowledge, this is the first study to interpret methylation heterogeneity in cancer from the perspective of coexpression perturbation. Our results provide new perspectives in tumor biology and may facilitate the identification of potential biomedical therapies for cancer treatment.

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“…Improper methylation status of the following genes has been identified thus far in laryngeal cancer: Retinoic acid receptor β (RARβ), death-associated protein kinase (DAPK), cyclin-dependent kinase inhibitor 2A (CDKN2A), MGMT, RASSF1A, fragile histidine triad, chromodomain-helicase-DNA-binding protein 5, cellular retinol binding protein 1 and HIC1 (12)(13)(14)(15)(16)(17)(18)(19). The majority of the studies reported certain correlations between the clinical course of the disease and the molecular changes identified.…”

Section: Discussionmentioning

confidence: 99%

Expression of the tumor suppressor gene hypermethylated in cancer 1 in laryngeal carcinoma

et al. 2015

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Abstract. Hypermethylated in cancer 1 (HIC1) is a putative suppressor gene, cooperating with TP53 in the regulation of apoptosis. The promoter site of this gene contains CpG islands susceptible to methylation. Altered methylation leads to the silencing of HIC1. Persistent loss of HIC1 function reflects the attenuation of proapoptotic characteristics of TP53 and may constitute the background for carcinogenesis. Altered methylation profiles along with diminished expression of HIC1 were documented in a number of solid neoplasms. The aim of this study was to evaluate the expression of the HIC1 gene in laryngeal carcinoma. RNA was extracted from samples of laryngeal cancer and corresponding healthy tissues of 21 patients with advanced laryngeal cancer (T3-T4). The amount of RNA (cDNA) was evaluated using reverse transcription-quantitative polymerase chain reaction with GADPH as the reference gene. Data demonstrated that HIC1 expression was significantly reduced in laryngeal cancer tissues. The relative expression of HIC1 was found to be ~40% lower in tumor samples compared to that in healthy controls. The median tumor/normal tissue ratio for HIC1 was 0.615. These results suggest that low HIC1 expression may be associated with neoplastic transformation in the larynx.

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Correlation between expression of cellular retinol-binding protein 1 and its methylation status in larynx cancer

Cited by 10 publications

References 23 publications

Comprehensive molecular exploration identified promoter DNA methylation of the CRBP1 gene as a determinant of radiation sensitivity in rectal cancer

Comprehensive molecular exploration identified promoter DNA methylation of the CRBP1 gene as a determinant of radiation sensitivity in rectal cancer

Heterogeneous DNA methylation contributes to tumorigenesis through inducing the loss of coexpression connectivity in colorectal cancer

Expression of the tumor suppressor gene hypermethylated in cancer 1 in laryngeal carcinoma

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