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lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer.
- Source :
-
Oncology reports [Oncol Rep] 2016 Nov; Vol. 36 (5), pp. 2960-2966. Date of Electronic Publication: 2016 Sep 22. - Publication Year :
- 2016
-
Abstract
- Esophageal cancer (EC) is one of the most common gastrointestinal cancers, which leads to the sixth ranking of cancer-related death. Long non-coding RNAs (lncRNAs) play pivotal roles in many biological processes. lncRNA human urothelial carcinoma associated 1 (UCA1) is significantly upregulated and functions as an important oncogene in many types of human cancers. However, the role of UCA1 in EC and its underlying mechanism remains unclear. In the present study, we demonstrated that UCA1 was significantly upregulated in EC tissues and associated with poor prognosis. Overexpression of UCA1 promoted the proliferation of EC cells, while silence of UCA1 inhibited EC cells growth. Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to Sox4 3'UTR, which suppressed the degradation of Sox4 mRNA by miR-204. This study provides the first evidence that UCA1 promotes cell proliferation through Sox4 in EC, suggesting that UCA1 and Sox4 may be potential therapeutic targets for EC.
- Subjects :
- Apoptosis genetics
Biomarkers, Tumor biosynthesis
Biomarkers, Tumor genetics
Cell Line, Tumor
Cell Transformation, Neoplastic
Esophageal Neoplasms pathology
Gene Expression Regulation, Neoplastic
Humans
MicroRNAs genetics
RNA, Long Noncoding genetics
SOXC Transcription Factors genetics
Transcriptional Activation
Cell Proliferation genetics
Esophageal Neoplasms genetics
MicroRNAs biosynthesis
RNA, Long Noncoding biosynthesis
SOXC Transcription Factors biosynthesis
Subjects
Details
- Language :
- English
- ISSN :
- 1791-2431
- Volume :
- 36
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Oncology reports
- Publication Type :
- Academic Journal
- Accession number :
- 27667646
- Full Text :
- https://doi.org/10.3892/or.2016.5121