Protein-coding genes combined with long non-coding RNAs predict prognosis in esophageal squamous cell carcinoma patients as a novel clinical multi-dimensional signature

2016 ◽  
Vol 12 (11) ◽  
pp. 3467-3477 ◽  
Author(s):  
Jin-Cheng Guo ◽  
Chun-Quan Li ◽  
Qiu-Yu Wang ◽  
Jian-Mei Zhao ◽  
Ji-Yu Ding ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Mortality Rate ◽  
Esophageal Squamous Cell Carcinoma ◽  
Esophageal Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Gastrointestinal Cancers ◽  
Protein Coding ◽  
Protein Coding Genes ◽  
Non Coding Rnas

Esophageal carcinoma is one of the most malignant gastrointestinal cancers worldwide, and has a high mortality rate.

scholarly journals Identification of key pathways regulated by a set of competitive long non-coding RNAs in oral squamous cell carcinoma

2019 ◽  
Vol 47 (4) ◽  
pp. 1758-1765 ◽  
Author(s):  
Zhifeng Yang ◽  
Zili Liu ◽  
Lingqiu Meng ◽  
Shuyan Ma
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Protein Coding ◽  
Protein Coding Genes ◽  
Non Coding Rnas ◽  
Key Pathways ◽  
Competitive Endogenous Rna

Objective The aim of this study was to identify important pathways regulated by a set of long non-coding RNAs (lncRNAs) in oral squamous cell carcinoma (OSCC). Methods A lncRNA-mediated competitive endogenous RNA network (LMCN) was constructed using information on microRNA (miRNA)–mRNA interactions and lncRNA–miRNA intersections from the E-GEOD-37991 transcription profiling data in the ArrayExpress database. A random walk with restart ranking algorithm was then applied to evaluate the influences of protein-coding genes regulated by competitive lncRNAs. Pathway enrichment scores were calculated based on the propagation scores of protein-coding genes. Finally, permutation tests were used to estimate the significance of the pathways. Results We obtained lncRNA–mRNA interactions based on miRNAs common to both miRNA–mRNA interactions and lncRNA–miRNA intersections, and used interactions with a z-score > 0.7 to construct a LMCN. Ten lncRNAs were identified as source nodes in the LMCN, and nine pathways with enrichment scores >0.8, including ‘Cell cycle’, ‘Endocytosis’, and ‘Pathways in cancer’, were significantly enriched by these source nodes. Conclusions Nine significant pathways regulated by a set of competitive lncRNAs were identified in OSCC, which may play important roles in the development of OSCC via the cell cycle and endocytosis.

scholarly journals LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Lijun Wang ◽  
Xiaojun Wang ◽  
Pengwei Yan ◽  
Yatian Liu ◽  
Xuesong Jiang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Cure Rate ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Non Coding Rnas ◽  
New Treatment

To improve the survival rate and cure rate of patients, it is necessary to find a new treatment scheme according to the molecular composition of (ESCC) in esophageal squamous cell carcinoma. Long non-coding RNAs (lncRNAs) regulate the progression of ESCC by various pathophysiological pathways. We explored the possible function of the lncRNA LINC00261 (LINC00261) on cisplatin (DDP) resistance of ESCC and its relative molecular mechanisms. In the study, we found that LINC00261 was downregulated in ESCC tissues, cell lines, and DDP-resistant ESCC patients. Besides, overexpression of LINC00261 not only inhibited cell proliferation, and DDP resistance but also promotes cell apoptosis. Further mechanistic research showed that LINC00261 sponged miR-545-3p which was negatively correlated with the expression of LINC00261. In addition, functional experiments revealed that upregulation of miR-766-5p promoted proliferation and enhanced DDP resistance. Subsequently, MT1M was testified to be the downstream target gene of miR-545-3p. Rescue experiments revealed that overexpression of MT1M largely restores miR-545-3p mimics-mediated function on ESCC progression. Our results demonstrate that the LINC00261 suppressed the DDP resistance of ESCC through miR-545-3p/MT1M axis.

scholarly journals Auraptene Attenuates Malignant Properties of Esophageal Stem-Like Cancer Cells

2016 ◽  
Vol 16 (4) ◽  
pp. 519-527 ◽  
Author(s):  
Saffiyeh Saboor-Maleki ◽  
Fatemeh B. Rassouli ◽  
Maryam M. Matin ◽  
Mehrdad Iranshahi
Keyword(s):  
Polymerase Chain Reaction ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Esophageal Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cells ◽  
Real Time ◽  
Squamous Cell ◽  
Chain Reaction ◽  
Polymerase Chain

The high incidence of esophageal squamous cell carcinoma has been reported in selected ethnic populations including North of Iran. Low survival rate of esophageal carcinoma is partially due to the presence of stem-like cancer cells with chemotherapy resistance. In the current study, we aimed to determine the effects of auraptene, an interesting dietary coumarin with various biological activities, on malignant properties of stem-like esophageal squamous cell carcinoma, in terms of sensitivity to anticancer drugs and expression of specific markers. To do so, the half maximal inhibitory concentration values of auraptene, cisplatin, paclitaxel, and 5-fluorouracil were determined on esophageal carcinoma cells (KYSE30 cell line). After administrating combinatorial treatments, including nontoxic concentrations of auraptene + cisplatin, paclitaxel, or 5-fluorouracil, sensitivity of cells to chemical drugs and also induced apoptosis were assessed. In addition, quantitative real-time polymerase chain reaction was used to study changes in the expression of tumor suppressor proteins 53 and 21 ( P53 and P21), cluster of differentiation 44 ( CD44), and B cell-specific Moloney murine leukemia virus integration site 1 ( BMI-1) upon treatments. Results of thiazolyl blue assay revealed that auraptene significantly ( P < .05) increased toxicity of cisplatin, paclitaxel, and 5-fluorouracil in KYSE30 cells, specifically 72 hours after treatment. Conducting an apoptosis assay using flow cytometry also confirmed the synergic effects of auraptene. Results of quantitative real-time polymerase chain reaction revealed significant ( P < .05) upregulation of P53 and P21 upon combinatorial treatments and also downregulation of CD44 and BMI-1 after auraptene administration. Current study provided evidence, for the first time, that auraptene attenuates the properties of esophageal stem-like cancer cells through enhancing sensitivity to chemical agents and reducing the expression of CD44 and BMI-1 markers.

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