Long noncoding RNA XIST promotes proliferation and invasion by targeting miR-141 in papillary thyroid carcinoma
Authors Xu Y, Wang J, Wang J
Received 7 April 2018
Accepted for publication 18 May 2018
Published 21 August 2018 Volume 2018:11 Pages 5035—5043
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Arseniy Yuzhalin
Yawei Xu,1 Junrong Wang,2 Junling Wang1
1College of Bioengineering, Jilin Agricultural Science and Technology University, Jilin City 132101, People’s Republic of China; 2Department of Gynaecology and Obstetrics, China-Japan Union Hospital of Jinlin University, Changchun 130033, People’s Republic of China
Background: The long noncoding RNA X-inactive specific transcript (XIST) was reported to play vital roles in tumor progression. In the present study, we determined the regulatory function of XIST in papillary thyroid carcinoma (PTC).
Materials and methods: XIST expression was determined in PTC tissues and cell lines by quantitative real-time polymerase chain reaction (PCR) (qRT-PCR). Cellular proliferation, migration, and invasion were measured using the Cell Counting Kit-8 (CCK-8) assay, wound-healing assay, and transwell invasion assay, respectively. Western blotting was used to determine protein expression. The downstream target miRNAs for XIST were identified by luciferase reporter assay and qRT-PCR.
Results: Relative expression of XIST was upregulated in PTC tissues and cell lines. High XIST expression was positively correlated with TNM stage and lymph node metastasis. Function assay demonstrated that knockdown of XIST significantly decreased cell proliferation, migration, and invasion in PTC cells. Moreover, we showed that the effects of XIST on PTC cell progression were mediated by miR-141.
Conclusion: Our results demonstrated that XIST functioned as an oncogene in PTC progression by regulating miR-141, suggesting that XIST might be a promising therapeutic target for PTC treatment.
Keywords: papillary thyroid carcinoma, XIST, miR-141, proliferation
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