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Transcribed ultraconserved noncoding RNAs (T-UCR) are involved in Barrett's esophagus carcinogenesis.

Fassan M, Dall'Olmo L, Galasso M, Braconi C, Pizzi M, Realdon S, Volinia S, Valeri N, Gasparini P, Baffa R, Souza RF, Vicentini C, D'Angelo E, Bornschein J, Nuovo GJ, Zaninotto G, Croce CM, Rugge M - Oncotarget (2014)

Bottom Line: A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-).Analogous BE-specific T-UCR profiles were shared by human and murine lesions.This study is the first demonstration of a role for T-UCRs in the transformation of Barrett's mucosa.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine (DIMED), Surgical Pathology & Cytopathology Unit, University of Padua, Padua, Italy. Department of Surgical Oncology and Gastroenterological Sciences (DiSCOG), University of Padua, Padua, Italy. Comprehensive Cancer Center, Ohio State University, Columbus, OH.

ABSTRACT
Barrett's esophagus (BE) involves a metaplastic replacement of native esophageal squamous epithelium (Sq) by columnar-intestinalized mucosa, and it is the main risk factor for Barrett-related adenocarcinoma (BAc). Ultra-conserved regions (UCRs) are a class non-coding sequences that are conserved in humans, mice and rats. More than 90% of UCRs are transcribed (T-UCRs) in normal tissues, and are altered at transcriptional level in tumorigenesis. To identify the T-UCR profiles that are dysregulated in Barrett's mucosa transformation, microarray analysis was performed on a discovery set of 51 macro-dissected samples obtained from 14 long-segment BE patients. Results were validated in an independent series of esophageal biopsy/surgery specimens and in two murine models of Barrett's esophagus (i.e. esophagogastric-duodenal anastomosis). Progression from normal to BE to adenocarcinoma was each associated with specific and mutually exclusive T-UCR signatures that included up-regulation of uc.58-, uc.202-, uc.207-, and uc.223- and down-regulation of uc.214+. A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-). Analogous BE-specific T-UCR profiles were shared by human and murine lesions. This study is the first demonstration of a role for T-UCRs in the transformation of Barrett's mucosa.

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Related in: MedlinePlus

uc.158- and uc.472- are overexpressed in Barrett's mucosaConfirming microarray and qRT-PCR data, Barrett's mucosa consistently showed uc.158- and uc.472- overexpression by comparison with squamous esophageal epithelium on in situ hybridization analysis. Scale bars, 100 μm; original magnifications, 10x and 20x.
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Figure 2: uc.158- and uc.472- are overexpressed in Barrett's mucosaConfirming microarray and qRT-PCR data, Barrett's mucosa consistently showed uc.158- and uc.472- overexpression by comparison with squamous esophageal epithelium on in situ hybridization analysis. Scale bars, 100 μm; original magnifications, 10x and 20x.

Mentions: The up-regulation of uc.158- and uc.472- was confirmed by ISH in a series of 5 esophagectomy specimens (Figure 2). The two T-UCRs revealed both a nuclear and a cytoplasmic expression (with perinuclear reinforcement). Increased uc.158- expression was detected in 5 out of 5 BE specimens compared with matched Sq. As for uc.472-, this was moderately expressed in all 5 BE specimens, while Sq was weakly positive in the basal and suprabasal cell compartments.


Transcribed ultraconserved noncoding RNAs (T-UCR) are involved in Barrett's esophagus carcinogenesis.

Fassan M, Dall'Olmo L, Galasso M, Braconi C, Pizzi M, Realdon S, Volinia S, Valeri N, Gasparini P, Baffa R, Souza RF, Vicentini C, D'Angelo E, Bornschein J, Nuovo GJ, Zaninotto G, Croce CM, Rugge M - Oncotarget (2014)

uc.158- and uc.472- are overexpressed in Barrett's mucosaConfirming microarray and qRT-PCR data, Barrett's mucosa consistently showed uc.158- and uc.472- overexpression by comparison with squamous esophageal epithelium on in situ hybridization analysis. Scale bars, 100 μm; original magnifications, 10x and 20x.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4196192&req=5

Figure 2: uc.158- and uc.472- are overexpressed in Barrett's mucosaConfirming microarray and qRT-PCR data, Barrett's mucosa consistently showed uc.158- and uc.472- overexpression by comparison with squamous esophageal epithelium on in situ hybridization analysis. Scale bars, 100 μm; original magnifications, 10x and 20x.
Mentions: The up-regulation of uc.158- and uc.472- was confirmed by ISH in a series of 5 esophagectomy specimens (Figure 2). The two T-UCRs revealed both a nuclear and a cytoplasmic expression (with perinuclear reinforcement). Increased uc.158- expression was detected in 5 out of 5 BE specimens compared with matched Sq. As for uc.472-, this was moderately expressed in all 5 BE specimens, while Sq was weakly positive in the basal and suprabasal cell compartments.

Bottom Line: A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-).Analogous BE-specific T-UCR profiles were shared by human and murine lesions.This study is the first demonstration of a role for T-UCRs in the transformation of Barrett's mucosa.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine (DIMED), Surgical Pathology & Cytopathology Unit, University of Padua, Padua, Italy. Department of Surgical Oncology and Gastroenterological Sciences (DiSCOG), University of Padua, Padua, Italy. Comprehensive Cancer Center, Ohio State University, Columbus, OH.

ABSTRACT
Barrett's esophagus (BE) involves a metaplastic replacement of native esophageal squamous epithelium (Sq) by columnar-intestinalized mucosa, and it is the main risk factor for Barrett-related adenocarcinoma (BAc). Ultra-conserved regions (UCRs) are a class non-coding sequences that are conserved in humans, mice and rats. More than 90% of UCRs are transcribed (T-UCRs) in normal tissues, and are altered at transcriptional level in tumorigenesis. To identify the T-UCR profiles that are dysregulated in Barrett's mucosa transformation, microarray analysis was performed on a discovery set of 51 macro-dissected samples obtained from 14 long-segment BE patients. Results were validated in an independent series of esophageal biopsy/surgery specimens and in two murine models of Barrett's esophagus (i.e. esophagogastric-duodenal anastomosis). Progression from normal to BE to adenocarcinoma was each associated with specific and mutually exclusive T-UCR signatures that included up-regulation of uc.58-, uc.202-, uc.207-, and uc.223- and down-regulation of uc.214+. A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-). Analogous BE-specific T-UCR profiles were shared by human and murine lesions. This study is the first demonstration of a role for T-UCRs in the transformation of Barrett's mucosa.

Show MeSH
Related in: MedlinePlus