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Knockdown of long non‐coding RNA XIST suppresses nasopharyngeal carcinoma progression by activating miR‐491‐5p
Author(s) -
Cheng Qiang,
Xu Xiuyin,
Jiang Hui,
Xu Lingen,
Li Qiang
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26535
Subject(s) - xist , gene knockdown , nasopharyngeal carcinoma , long non coding rna , biology , microrna , oncogene , cancer research , competing endogenous rna , cell growth , downregulation and upregulation , microbiology and biotechnology , cell culture , cell , x inactivation , gene , genetics , medicine , x chromosome , cell cycle , radiation therapy
Dysregulated long non‐coding RNAs (lncRNAs) and microRNAs (miRNAs) play key roles in the development and progression of human cancers. X‐inactive specific transcript (XIST), an lncRNA, is known as an oncogene in multiple tumors. However, the roles of XIST and its related miRNAs in nasopharyngeal carcinoma (NPC) are poorly understood. In this study, we found that XIST expression was significantly upregulated in NPC tissues and cell lines. Knockdown of XIST inhibited NPC cell proliferation and invasion and induced apoptosis in vitro, as well as suppressed NPC tumor growth in vivo. Further analysis revealed that XIST and miR‐491‐5p interact with and repress each other. XIST may function as an endogenous miR‐491‐5p sponge to regulate the target gene of miR‐491‐5p. Taken together, these results provide a comprehensive view of the XIST/miR‐491‐5p axis in human NPC cells and may provide a new therapeutic target for treating NPC.