RuvBl2 cooperates with Ets2 to transcriptionally regulate hTERT in colon cancer

Flavin, Padraic; Redmond, Aisling M.; McBryan, Jean; Cocchiglia, Sinéad; Tibbitts, Paul; Fahy-Browne, Patrick; Kay, Elaine W.; Treumann, Achim; Perrem, Kilian; McIlroy, Marie; Hill, Arnold D.; Young, Leonie S.

doi:10.1016/j.febslet.2011.07.005

Cited by 22 publications

(20 citation statements)

References 48 publications

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“…Also RUVBL2 promotes tumorigenicity, is required for cell viability in hepatocellular, renal and breast cancers (Osaki et al., 2013) and is inversely associated with tumor differentiation grade and considered a marker of poor prognosis (Rousseau et al., 2007). In our cell models, RUVBL2 was highly expressed in more aggressive cells and advanced CRCs, in sharp and inverse relationship with PPARγ in line also with in vivo data (Flavin et al., 2011).…”

Section: Discussionsupporting

confidence: 88%

Proteomic characterization of peroxisome proliferator‐activated receptor‐γ (PPARγ) overexpressing or silenced colorectal cancer cells unveils a novel protein network associated with an aggressive phenotype

et al. 2016

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were shared by the two cell models with opposite expression levels, suggesting a possible regulation by PPARg. mRNA and western blot analysis were undertaken to obtain a technical validation and confirm the expression trend observed by 2-D DIGE data. We associated EZR upregulation with increased cell surface localization in PPARg-overexpressing cells by flow cytometry and immunofluorescence staining. We also correlated EZR and PPARg expression in our series of CRC specimens and the expression profiling of all five proteins levels in the publicly available colon cancer genomic data from Oncomine and Cancer Genome Atlas (TCGA) colon adenocarcinoma (COAD) datasets. In summary, we

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Section: Discussionsupporting

confidence: 88%

Proteomic characterization of peroxisome proliferator‐activated receptor‐γ (PPARγ) overexpressing or silenced colorectal cancer cells unveils a novel protein network associated with an aggressive phenotype

et al. 2016

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“…Importantly, TNF significantly upregulated the expression of Ascl2, a Wnt target gene and key ISC transcription factor(19) in a dose-dependent manner (Fig 3A). TNF also upregulated the Ascl2 target gene Ets2(20) and Wnt-target CD44, both of which are implicated in stem cell maintenance and suppression of differentiation. TNF treatment did not alter the mRNA expression of differentiation markers (AP, Muc2, TFF3, Lys, CK20) or markers of proliferation (Ki67 and PCNA).…”

Section: Resultsmentioning

confidence: 99%

Epithelial TNF Receptor Signaling Promotes Mucosal Repair in Inflammatory Bowel Disease

Bradford

Ryu

Singh

et al. 2017

The Journal of Immunology

111

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TNF plays an integral role in inflammatory bowel disease (IBD) as evidenced by the dramatic therapeutic responses in Crohn’s disease (CD) patients induced by chimeric anti-TNF mAbs. However, treatment of CD patients with etanercept, a decoy receptor that binds soluble TNF, fails to improve disease. To explore this discrepancy, we interrogated the role of TNF signaling on Wnt/β-catenin-mediated intestinal stem and progenitor cell (ISC/PC) expansion in CD patients, human cells, and preclinical mouse models. We hypothesized that TNF exerts beneficial effects on intestinal epithelial cell (IEC) responses to injury. In CD patients, ISC/PC Wnt/β-catenin signaling correlates with inflammation status. TNF-deficient (Tnf−/−) mice exhibited increased apoptosis, less IEC proliferation, and less Wnt signaling when stimulated with anti-CD3 mAb. Bone marrow chimera (BMC) mice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression by radioresistant IEC. WT-> Tnfr1/2−/− BMC mice given chronic DSS colitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/β-catenin signaling, consistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing. The direct effect of TNF on stem cells was demonstrated by studies of TNF-induced Wnt/β-catenin target gene expression in murine enteroids and colonoid cultures and TNF-induced β-catenin activation in non-transformed human NCM460 cells (TOPFlash) and mice (TOP-GAL). Together these data support the hypothesis that TNF plays a beneficial role in enhancing Wnt/β-catenin signaling during ulcer healing in IBD. These novel findings will inform clinicians and therapeutic chemists alike as they strive to develop novel therapies for IBD patients.

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“…The expressions of these proteins are thought to be increased in many types of cancer (19). Flavin et al (12) showed positive reptin expression in 60% of colon cancer samples in their study. In this study, mean reptin mRNA expressions were also significantly higher in tumour tissues than in normal tissues in both total and breast cancer patients.…”

Section: Discussionmentioning

confidence: 79%

“…Most malignant cancers (85-90%) are known to show high telomerase activity for cellular immortality (12). Although the absence of telomerase in normal cells is considered a natural defence against the development of cancer, telomerase is thought to reappear in cancer cells through multiple mechanisms (13).…”

Section: Discussionmentioning

confidence: 99%

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Normal and Tumour Tissue mRNA Expressions of Telomerase Complex Genes in Several Types of Cancer

Can¹,

Atalay²,

Miser-Salihoglu³

et al. 2017

Balkan Med J

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Aims:To investigate the changes in mRNA expression levels of telomerase-related significant proteins in several types of cancer.Methods:Human telomerase reverse transcriptase, pontin, reptin and dyskerin expressions were measured in normal and tumour tissues obtained from 26 patients with colorectal, breast and gastric cancers, using the real-time reverse transcriptase-polymerase chain reaction method.Results:For all patients, no significant difference was found in mRNA expressions of human telomerase reverse transcriptase and dyskerin (p>0.05), although their levels in tumour tissues were found to be higher than in normal tissues. However, pontin and reptin mRNA expressions were significantly higher in tumour tissues than in normal tissues (p<0.01). While human telomerase reverse transcriptase showed a high correlation with only pontin (p<0.001) in normal tissues, high positive correlations were observed between human telomerase reverse transcriptase with pontin (p<0.005), reptin (p<0.01) and dyskerin (p<0.01) in tumour tissues.Conclusion:The increased mRNA expressions of all four genes in tumour tissues may suggest a role in cancer development. Correlations of pontin, reptin and dyskerin with human telomerase reverse transcriptase support the hypotheses describing their roles in telomerase complexes.

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RuvBl2 cooperates with Ets2 to transcriptionally regulate hTERT in colon cancer

Cited by 22 publications

References 48 publications

Proteomic characterization of peroxisome proliferator‐activated receptor‐γ (PPARγ) overexpressing or silenced colorectal cancer cells unveils a novel protein network associated with an aggressive phenotype

Proteomic characterization of peroxisome proliferator‐activated receptor‐γ (PPARγ) overexpressing or silenced colorectal cancer cells unveils a novel protein network associated with an aggressive phenotype

Epithelial TNF Receptor Signaling Promotes Mucosal Repair in Inflammatory Bowel Disease

Normal and Tumour Tissue mRNA Expressions of Telomerase Complex Genes in Several Types of Cancer

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