scholarly journals Aberrantly upregulated FAM83H‑AS1 facilitates malignant progression of esophageal squamous cell carcinoma

2020 ◽  
Vol 20 (6) ◽  
pp. 1-1
Author(s):  
Lijia Bu ◽  
Rong Wang ◽  
Pingping Liu ◽  
Jie Da
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Malignant Progression

scholarly journals Unbalanced YAP–SOX9 circuit drives stemness and malignant progression in esophageal squamous cell carcinoma

Oncogene ◽  
2018 ◽  
Vol 38 (12) ◽  
pp. 2042-2055 ◽  
Author(s):  
Lianghai Wang ◽  
Zhiyu Zhang ◽  
Xiaodan Yu ◽  
Xuan Huang ◽  
Zheng Liu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Malignant Progression

scholarly journals CircCNTNAP3-TP53-positive feedback loop suppresses malignant progression of esophageal squamous cell carcinoma

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Hui Wang ◽  
Xuming Song ◽  
Yajing Wang ◽  
Xuewen Yin ◽  
Yingkuan Liang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Malignant Progression ◽  
Gene Transcript ◽  
Wild Type ◽  
Positive Feedback Loop

AbstractMutation or downregulation of p53 (encoded by TP53) accelerates tumorigenesis and malignant progression in esophageal squamous cell carcinoma (ESCC). However, it is still unknown whether circular RNAs (circRNAs), a novel class of endogenous noncoding RNAs, participate in the regulation of this progress. In this study, we explored the expression profiles of circRNAs in three paired samples of ESCC and identified cCNTNAP3, which is a circRNA that originates from the CNTNAP3 gene transcript and is highly expressed in normal human esophageal tissue. However, we found that the cCNTNAP3 expression level was significantly downregulated in ESCC tissues. In vitro and in vivo studies revealed that cCNTNAP3 inhibited proliferation and increased apoptosis in p53 wild-type ESCC cells, but not in mutant cells. Mechanistically, we found that cCNTNAP3 promotes the expression of p53 by sponging miR-513a-5p. Rescue assay confirmed that the suppressive function of cCNTNAP3 was dependent on miR-513a-5p. We also observed that p53/RBM25 participated in the formation of cCNTNAP3, which implied the existence of a positive feedback loop between cCNTNAP3 and p53. Furthermore, the downregulation of cCNTNAP3 was significantly correlated with later T stage and thus can serve as an independent risk factor for the overall survival of patients with p53 wild-type ESCC. In conclusion, the cCNTNAP3-TP53 positive feedback loop may provide a potential target for the management of ESCC, which also reveals the important role of circRNAs in the regulation of p53.

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