Heterogeneous expression and association of β‐catenin, p16 and c‐myc in multistage colorectal tumorigenesis and progression detected by tissue microarray

Xie, Dan; Sham, Jst; Zeng, Wei; Lin, Han; Li, Hong; Wu, Hui; Wen, Jian Ming; Fang, Yan; Hu, Liang; Guan, Xin Yuan

doi:10.1002/ijc.11514

Cited by 97 publications

(73 citation statements)

References 30 publications

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“…Details are described in the Supporting Materials and Methods. 11 Immunofluorescence. Details are described in the Supporting Materials and Methods.…”

Section: Methodsmentioning

confidence: 99%

Down-Regulation of Tyrosine Aminotransferase at A Frequently Deleted Region 16Q22 Contributes to the Pathogenesis of Hepatocellular Carcinoma

Dong²,

Xie³

et al. 2010

Hepatology

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Loss of 16q is one of the most frequent alterations in many malignancies including hepatocellular carcinomas (HCC), suggesting the existence of a tumor suppressor gene (TSG) within the frequently deleted region. In this report we describe the identification and characterization of one candidate TSG, tyrosine aminotransferase gene (TAT), at 16q22.1. Loss of one TAT allele was detected in 27/50 (54%) of primary HCCs by quantitative real-time polymerase chain reaction. In addition, homo-deletion of TAT alleles was detected in two cases. Down-regulation of TAT was detected in 28/50 (56%) of HCCs, which was significantly associated with the loss of TAT allele and hypermethylation of TAT 5 0 CpG island (CGI) region (P < 0.001). Functional studies found that TAT has a strong tumor suppressive ability. Introduction of the TAT gene into HCC cell lines could effectively inhibit colony formation in soft agar, foci formation, and tumor formation in nude mice. Further study found that the tumor suppressive mechanism of TAT was associated with its proapoptotic role in a mitochondrial-dependent manner by promoting cytochrome-c release and activating caspase-9 and PARP. Conclusion: Taken together, our findings suggest that TAT plays an important suppressive role in the development and progression of HCC.

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“…Details are described in the Supporting Materials and Methods. 11 Immunofluorescence. Details are described in the Supporting Materials and Methods.…”

Section: Methodsmentioning

confidence: 99%

Down-Regulation of Tyrosine Aminotransferase at A Frequently Deleted Region 16Q22 Contributes to the Pathogenesis of Hepatocellular Carcinoma

Dong²,

Xie³

et al. 2010

Hepatology

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“…The TMA was constructed according to a method described previously [21]. Briefly, the individual donor tissue block and the corresponding histological H&E stained slides were overlaid for tissue TMA sampling.…”

Section: Methodsmentioning

confidence: 99%

Intensive expression of Bmi-1 is a new independent predictor of poor outcome in patients with ovarian carcinoma

Yang

Cai

et al. 2010

BMC Cancer

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BackgroundIt has been suggested that the B-cell specific moloney leukemia virus insertion site 1 (Bmi-1) gene plays an oncogenic role in several types of human cancer, but the status of Bmi-1 amplification and expression in ovarian cancer and its clinical/prognostic significance are unclear.MethodsThe methods of immunohistochemistry and fluorescence in situ hybridization were utilized to examine protein expression and amplification of Bmi-1 in 30 normal ovaries, 30 ovarian cystadenomas, 40 borderline ovarian tumors and 179 ovarian carcinomas.ResultsIntensive expression of Bmi-1 was detected in none of the normal ovaries, 3% cystadenomas, 10% borderline tumors, and 37% ovarian carcinomas, respectively. Amplification of Bmi-1 was detected in 8% of ovarian carcinomas. In ovarian carcinomas, significant positive associations were found between intensive expression of Bmi-1 and the tumors ascending histological grade, later pT/pN/pM and FIGO stages (P < 0.05). In univariate survival analysis of the ovarian carcinoma cohorts, a significant association of intensive expression of Bmi-1 with shortened patient survival (mean 49.3 months versus 100.3 months, p < 0.001) was demonstrated. Importantly, Bmi-1 expression provided significant independent prognostic parameters in multivariate analysis (p = 0.005).ConclusionsThese findings provide evidence that intensive expression of Bmi-1 might be important in the acquisition of an invasive and/or aggressive phenotype of ovarian carcinoma, and serve as a independent biomarker for shortened survival time of patients.

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“…A NPC-tissue microarray was constructed as previously described (Xie et al, 2003). Clinico-pathological characteristics of the NPC patients are summarized in Table 1.…”

Section: Npc Patients and Tissue Microarraymentioning

confidence: 99%

EZH2 supports nasopharyngeal carcinoma cell aggressiveness by forming a co-repressor complex with HDAC1/HDAC2 and Snail to inhibit E-cadherin

et al. 2011

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The enhancer of zeste homolog 2 (EZH2) is upregulated and has an oncogenic role in several types of human cancer. However, the abnormalities of EZH2 and its underlying mechanisms in the pathogenesis of nasopharyngeal carcinoma (NPC) remain unknown. In this study, we found that high expression of EZH2 in NPC was associated closely with an aggressive and/or poor prognostic phenotype (Po0.05). In NPC cell lines, knockdown of EZH2 by short hairpin RNA was sufficient to inhibit cell invasiveness/metastasis both in vitro and in vivo, whereas ectopic overexpression of EZH2 supported NPC cell invasive capacity with a decreased expression of E-cadherin. In addition, ablation of endogenous Snail in NPC cells virtually totally prevented the repressive activity of EZH2 to E-cadherin, indicating that Snail might be a predominant mediator of EZH2 to suppress E-cadherin. Furthermore, co-immunoprecipitation (IP), chromatin IP and luciferase reporter assays demonstrated that in NPC cells, (1) EZH2 interacted with HDAC1/HDAC2 and Snail to form a repressive complex; (2) these components interact in a linear fashion, not in a triangular fashion, that is, HDAC1 or HDAC2 bridge the interaction between EZH2 and Snail; and (3) the EZH2/HDAC1/2/Snail complex could closely bind to the E-cadherin promoter by Snail, but not YY1, to repress E-cadherin. The data provided in this report suggest a critical role of EZH2 in the control of cell invasion and/or metastasis by forming a co-repressor complex with HDAC1/HDAC2/Snail to repress E-cadherin, an activity that might be responsible, at least in part, for the development and/or progression of human NPCs.

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Heterogeneous expression and association of β‐catenin, p16 and c‐myc in multistage colorectal tumorigenesis and progression detected by tissue microarray

Cited by 97 publications

References 30 publications

Down-Regulation of Tyrosine Aminotransferase at A Frequently Deleted Region 16Q22 Contributes to the Pathogenesis of Hepatocellular Carcinoma

Down-Regulation of Tyrosine Aminotransferase at A Frequently Deleted Region 16Q22 Contributes to the Pathogenesis of Hepatocellular Carcinoma

Intensive expression of Bmi-1 is a new independent predictor of poor outcome in patients with ovarian carcinoma

EZH2 supports nasopharyngeal carcinoma cell aggressiveness by forming a co-repressor complex with HDAC1/HDAC2 and Snail to inhibit E-cadherin

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