Poly (C)-binding protein 2 (PCBP2) promotes the progression of esophageal squamous cell carcinoma (ESCC) through regulating cellular proliferation and apoptosis

2016 ◽  
Vol 212 (8) ◽  
pp. 717-725 ◽  
Author(s):  
Jinjun Ye ◽  
Guoren Zhou ◽  
Zhi Zhang ◽  
Lei Sun ◽  
Xia He ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cellular Proliferation ◽  
Binding Protein ◽  
Proliferation And Apoptosis

scholarly journals Upregulation of microRNA-98 increases radiosensitivity in esophageal squamous cell carcinoma

2016 ◽  
Vol 57 (5) ◽  
pp. 468-476 ◽  
Author(s):  
Ying-Ying Jin ◽  
Qing-Juan Chen ◽  
Yang Wei ◽  
Ya-Li Wang ◽  
Zhong-Wei Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cellular Proliferation ◽  
Luciferase Assay ◽  
Survival Fraction ◽  
Aberrant Expression ◽  
Functional Analyses ◽  
Esophageal Cancer Cells

Abstract Although radiation resistance is a common challenge in the clinical treatment of esophageal squamous cell carcinoma (ESCC), an effective treatment strategy has yet to be developed. Aberrant expression of microRNAs (miRNAs) is responsible for cancer sensitivity to radiation. In this study, we aimed to identify the miRNAs that are associated with radioresistance in ESCC. We used a miRNA microarray to perform a comparison of miRNA expression in both ESCC parental and acquired radioresistance cell lines. qRT-PCR was used to confirm the alterations. Cell radiosensitivity was determined with a survival fraction assay. Functional analyses of the identified miRNA in ESCC cells with regard to metastasis and apoptosis were performed by transwell assays and flow cytometry. The miRNA targets were identified with pathway analysis and confirmed with a luciferase assay. miR-98 was recognized as the most downregulated miRNA in established radioresistant cell line. AmiR-98 mimic enforced the expression of miRNA-98 and made ESCC cells sensitive to radiotherapy, while anti-miR-98 reversed this process. Optimal results were achieved by decreasing cellular proliferation, decreasing cell migration and inducing apoptosis. The luciferase target gene analysis results showed that the overexpression of miRNA-98 inhibited tumor growth and resistance tolerance by directly binding to the BCL-2 gene. Our study indicated that increasing miRNA-98 expression can be used as a potential radiosensitive therapeutic strategy for treating esophageal cancer cells.

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