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Long non‑coding RNA DANCR promotes nasopharyngeal carcinoma cell proliferation and migration
Author(s) -
Ya Hao,
Hui Zhao,
Xiaojie Jin,
Ping He,
Jiafeng Zhang,
Qian Dong,
Weiwei Shi,
Miaomiao Zhao
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.9906
Subject(s) - biology , cell growth , nasopharyngeal carcinoma , gene knockdown , cell cycle , protein kinase b , cancer research , oncogene , cell migration , apoptosis , pten , cell , microbiology and biotechnology , pi3k/akt/mtor pathway , signal transduction , medicine , biochemistry , genetics , radiation therapy
Aberrant expression of numerous long non‑coding RNAs (lncRNAs) has been reported to be associated with nasopharyngeal carcinoma (NPC). The present study aimed to investigate the expression and function of lncRNA differentiation antagonizing non‑protein coding RNA (DANCR) in NPC pathogenesis. Reverse transcription‑quantitative polymerase chain reaction results suggested that DANCR was significantly upregulated in NPC cells. Overexpression of DANCR promoted 5‑8F cell proliferation and migration, as detected by Cell Counting Kit‑8, colony formation and wound healing assays. DANCR was additionally identified to inhibit apoptosis, as determined by flow cytometric analysis. Furthermore, DANCR knockdown suppressed cell proliferation and migration, and promoted cell apoptosis in SUNE‑1 cell. Western blot analysis suggested that DANCR regulated the phosphorylation of AKT serine/threonine kinase and the protein expression of PTEN in NPC cells. Knockdown of DANCR decreased tumor growth in a xenograft model following subcutaneous injection of SUNE‑1 cells. Collectively, the present results suggested that DANCR regulated the proliferation, migration and apoptosis of NPC cells.

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