MicroRNA-1322 regulatesECRG2allele specifically and acts as a potential biomarker in patients with esophageal squamous cell carcinoma

2012 ◽  
Vol 52 (8) ◽  
pp. 581-590 ◽  
Author(s):  
Tengfei Zhang ◽  
Dan Zhao ◽  
Qiming Wang ◽  
Xiying Yu ◽  
Yaling Cui ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Potential Biomarker

Assessment of serum concentrations of Dkk1 as potential biomarker for esophageal squamous cell carcinoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e15675-e15675
Author(s):  
C. Zer ◽  
X. Dong ◽  
K. Kernstine ◽  
L. Zhong
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Wnt Signaling Pathway ◽  
Predictive Marker ◽  
Serum Concentrations ◽  
Serum Samples ◽  
Double Blind ◽  
Potential Biomarker

e15675 Background: Esophageal squamous cell carcinoma (ESCC) is one of the most common fatal cancers worldwide due to the lack of an early disease screening strategy. Identification of diagnostic markers will greatly improve the morbid outcome. Dickkopf 1 (Dkk1) is a secreted antagonist of Wnt signaling pathway, an important pathway in tumorigenesis. The expressions of Dkk1 seem to be tumor-specific: reduced expressions have been seen in colorectal cancer, but elevated levels were reported for hepatoblastomas. In ESCC, the situation is less clear, for both elevation and reduction of Dkk1 were reported. The serum concentrations of Dkk1 have also been shown to be higher in ESCC patients’ sera in one study. In view of the varied outcome from Dkk1 tissue expressions and the scarce reports on Dkk1 serum concentration from ESCC patients, we therefore sought to determine the tissue expression and serum concentrations of Dkk1 as our first step to evaluate the potential of Dkk1 as a diagnostic marker for ESCC. Methods: The expression levels of Dkk1 in ten ESCC tumor and adjacent non-tumor tissues were examined by Western blot. Serum Dkk1 level of 168 samples were quantified in a double-blind fashion by ELISA (Dkk1 Duoset ELISA development kit from R & D Systems, Minneapolis, MN). To ensure that the serum Dkk1 detection was not affected by autoantibodies against Dkk1 present in sera, we also measured serum Dkk1 autoantibody levels by ELISA with modifications to the ELISA kit. Results: Seven out of ten of the tumors showed elevated Dkk1 level, while only two out of ten of the control normal tissue showed elevation. Surprisingly, after decoding of our serum samples into 80 patients and 88 normal controls, we found that Dkk1 level was significantly lower in patient sera (2.99ng/ml) than the normal samples (5.32ng/ml) (p=0.0001; t-test). The measurements were not obscured by the presence of Dkk1 autoantibodies, as they were not different between patient and control samples. Conclusions: Contrary to previous published results, we found Dkk1 is suppressed in patient sera, and thus our result undermines the potential of serum Dkk1 level as a predictive marker for ESCC. Further investigations will be needed to explain the discrepancies between the studies. No significant financial relationships to disclose.

scholarly journals A six-microRNA signature in plasma was identified as a potential biomarker in diagnosis of esophageal squamous cell carcinoma

Oncotarget ◽  
2017 ◽  
Vol 8 (21) ◽  
pp. 34468-34480 ◽  
Author(s):  
Xin Zhou ◽  
Wei Wen ◽  
Jun Zhu ◽  
Zebo Huang ◽  
Lan Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Potential Biomarker

scholarly journals RNA m6A demethylase FTO-mediated epigenetic up-regulation of LINC00022 promotes tumorigenesis in esophageal squamous cell carcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Yuanbo Cui ◽  
Chunyan Zhang ◽  
Shanshan Ma ◽  
Zhe Li ◽  
Wenjie Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epigenetic Modification ◽  
Epigenetic Mechanism ◽  
Potential Biomarker

Abstract Background Long non-coding RNA (LncRNA) controls cell proliferation and plays a significant role in the initiation and progression of esophageal squamous cell carcinoma (ESCC). N6-methyladenosine (m6A) modification now is recognized as a master driver of RNA function to maintain homeostasis in cancer cells. However, how m6A regulates LncRNA function and its role in tumorigenesis of ESCC remain unclear. Methods Multiple ESCC datasets were used to analyze gene expression in tumor tissues and normal tissues. Kaplan-Meier method and the ROC curve were conducted to evaluate the prognostic value and diagnostic value of LINC00022 in ESCC, respectively. Both gain-of-function and loss-of-function experiments were employed to investigate the effects of LINC00022 on ESCC growth in vitro and in vivo. Bioinformatics analysis, colorimetric m6A assay, RIP, MeRIP and co-IP was performed to explore the epigenetic mechanism of LINC00022 up-regulation in ESCC. Results Here we report that m6A demethylation of LncRNA LINC00022 by fat mass and obesity-associated protein (FTO) promotes tumor growth of ESCC in vivo. Clinically, we revealed that LINC00022 was up-regulated in primary ESCC samples and was predictive of poor clinical outcome for ESCC patients. Mechanistically, LINC00022 directly binds to p21 protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation. Further, the elevated FTO in ESCC decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. Over-expression of FTO was shown to drive LINC00022-dependent cell proliferation and tumor growth of ESCC. Conclusions Thus, this study demonstrated m6A-mediated epigenetic modification of LncRNA contributes to the tumorigenesis in ESCC and LINC00022, specific target of m6A, serves as a potential biomarker for this malignancy.

scholarly journals Preliminary evaluation for Bit1 as a potential biomarker for squamous cell carcinoma and adenocarcinoma of esophagus

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770826
Author(s):  
Jing Chen ◽  
Hongtao Liu ◽  
Pan Gao ◽  
Yiran Hui ◽  
Zhenzhen Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Matrix Metalloproteinase ◽  
Cell Carcinoma ◽  
Esophageal Adenocarcinoma ◽  
Squamous Cell ◽  
Expression Patterns ◽  
Matrix Metalloproteinase 2 ◽  
Potential Biomarker ◽  
Well Differentiated

Mounting evidence has demonstrated that Bit1 has been investigated as an etiological factor for certain cancers, including esophageal squamous cell carcinoma reported in our previous study, but data regarding possible roles of Bit1 in esophageal squamous cell carcinoma and esophageal adenocarcinoma remain to be elucidated. The purpose of this study was to examine whether Bit1 can be a novel diagnostic marker for the patients with esophageal squamous cell carcinoma and esophageal adenocarcinoma. The results revealed that Bit1 level in esophageal squamous cell carcinoma was significantly higher than that in esophageal adenocarcinoma tissues ( p < 0.05); notably, Bit1 level in esophageal adenocarcinoma tissues was lower than that in paired normal tissues but no difference was found ( p > 0.05). Bit1 expression patterns were completely in accordance with matrix metalloproteinase 2 and Bcl-2 in esophageal squamous cell carcinoma and esophageal adenocarcinoma. In addition, Bit1, Bcl-2, and matrix metalloproteinase 2 expression patterns in different differentiated esophageal squamous cell carcinoma were higher than those in corresponding normal esophageal tissues. Bit1 expression in poorly differentiated esophageal squamous cell carcinoma was significantly higher than that in normal esophageal tissues ( p < 0.05) but not in moderately and well-differentiated esophageal squamous cell carcinoma. Matrix metalloproteinase 2 expression patterns in poorly and moderately differentiated esophageal squamous cell carcinoma were significantly higher than those in corresponding normal esophageal tissues ( p < 0.01) but not in well-differentiated esophageal squamous cell carcinoma tissue ( p > 0.05). Bcl-2 expression patterns in various differentiated esophageal squamous cell carcinoma were higher than those in corresponding normal esophageal tissues with no statistical differences ( p > 0.05). Importantly, Bit1 expression was positively correlated with both matrix metalloproteinase 2 and Bcl-2 expression in esophageal squamous cell carcinoma and esophageal adenocarcinoma tissues ( p < 0.05). Collectively, these preliminary data support further investigation of Bit1 as an important diagnostic factor for esophageal squamous cell carcinoma and esophageal adenocarcinoma.

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